Pro-Inflammatory Cytokines Overview - UK (2022)

What are Pro-Inflammatory Cytokines?

Cytokine is a general term used for small secreted proteins that are key modulators of inflammation. Cytokines are produced in response to invading pathogens to stimulate, recruit, and proliferate immune cells. Cytokines includes interleukins (IL), chemokines, interferons, and tumor necrosis factors (TNF). Cytokines are subdivided based on the nature of the immune response and the source of their production (Table 1) [1].

On this page:

  • Role of pro-inflammatory cytokines
  • Pro-inflammatory cytokine regulation
  • References

There are both pro-inflammatory and anti-inflammatory cytokines. The pro-inflammatory cytokines are secreted from Th1 cells, CD4+ cells, macrophages, and dendritic cells. They are characterized by production of several Interleukins (IL), IL-1, IL-2, IL-12, IL-17, IL-18, IFN-γ, and TNF-α. The key pro-inflammatory cytokines are IL-1, IL-6, and TNF-α. These cytokines signal via type I cytokine receptors (CCR1) that are structurally divergent from other cytokine receptor types. They are crucial for coordinating cell mediated immune response and play a critical role in modulating the immune system. Pro-inflammatory cytokines generally regulate growth, cell activation, differentiation, and homing of the immune cells to the sites of infection with the aim to control and eradicate the intracellular pathogens, including viruses [1].

Key pro-inflammatory cytokines

IL-1

IL-1 is subdivided in IL-1α and IL-1β. IL-1β is potent pro-inflammatory cytokine, induced mainly by lymphocytes, macrophages, and monocytes in response to microbial molecules. Upon viral infection, the pattern recognition receptors (PPR) and toll-like receptors (TLRs) are expressed which in turn lead to enhanced expression of IL-1β. IL-1β stimulate CD4+ cells and differentiate them towards Th17 cells. In addition to the stimulatory effect of the IL-1 family, there are also members (IL-1R, a and 2) that can inhibit or suppress the IL-1 cytokine expression. IL-1Ra is secreted from neutrophils, macrophages, monocytes, and hepatocytes aiming to decrease the inflammation. However, the expression of IL-Ra needs to be expressed up to 1,000-fold in order to efficiently inhibit or suppress the expression of IL-1β [1].

IL-6

IL-6 is a pleiotropic cytokine that not only affects the immune system, but also acts in other biological systems and many physiological events, such as regulating cell growth, as well as gene activation, proliferation, survival, and differentiation. IL-6 is produced by a variety of cell types including monocytes, fibroblast, and endothelial cells. Upon stimulation, IL-6 is secreted by many additional cell types including macrophages, T cells, B cells, mast cells, glial cells, eosinophils, keratinocytes, and granulocytes. IL-6 stimulates several types of leukocytes and the production of acute phase proteins in the liver. It is particularly important in inducing B-cells to differentiate into antibody-forming cells (plasma cells). Binding of IL-6 to its receptor initiates cellular events including activation of JAK (Janus Kinase) kinases and activation of Ras-mediated signaling.

TNF-α

Like other Th1 pro-inflammatory cytokines, TNF-α has an important role comprising the inflammatory response both locally and in the circulation. TNF-α triggers the expression of vascular endothelial cells as well as enhances the leukocyte adhesion molecules that stimulate immune cell infiltration. It has a crucial role in early response against viral infection by enhancing the infiltration of lymphocyte to the site of infection [3, 4].

Chemokines

Chemokines are cytokines with chemotactic activities. They are classified into four main subfamilies including CXC, CC, CX3C, and XC chemokines with both structural and functional differences. They play a crucial role in regulating the movement and localization of lymphocytes and a subset of dendritic cells. The CXC chemokines are mainly involved in the recruitment of immune cells to the site of inflammation and the homeostatic chemokines that mediate homeostatic migration and homing of lymphocytes. However, some chemokines have also dual-function and can be inflammatory and/or anti-inflammatory depending on the site of expression and concentration [3].

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Figure 1. Cytokine network. Immune cells communicate with other immune cells by cytokines, which control proliferation, differentiation, and function. Furthermore, they are involved in processes of inflammation, hematopoiesis, neurogenesis, embryogenesis, and oncogenesis. Unlike hormones, cytokines are not stored in glands as pre-formed molecules but are rapidly synthesized and secreted mostly after stimulation. Cytokines frequently affect the action of other cytokines in an additive, synergistic, or antagonistic manner.

Table 1. Summary of selected cytokines and their functions.

CytokineClassificationMain SourcesReceptorTarget CellMajor Function
ErythropoietinEndotheliumEpoRStem cellsRed blood cell production
G-CSFPro-inflammatoryFibroblasts, endotheliumCD114Stem cells in BMGranulocyte production
GM-CSFAdaptive immunityT cells, macrophages, fibroblastsCD116, CDw131Stem cellsGrowth and differentiation of monocytes, and eosinophil, granulocytes production
IL-1Pro-inflammatoryMacrophages, B cells, DCsCD121aB cells, NK cells, T-cellsPyrogenic, pro-inflammatory, proliferation and differentiation, BM cell proliferation
IL-2Adaptive immunityTh1 cellsCD25Activated T and B cells, NK cellsProliferation of B cells, activated T cells, NK cell function
IL-3Adaptive immunityT cellsCD123, CDw131Stem cellsHematopoietic precursor proliferation and differentiation
IL-4Adaptive immunityTh CellsCD124B cell, T cell, macrophagesProliferation of B and cytotoxic T cells, enhances MHC class II expression, stimulates IgG and IgE production
IL-5Adaptive immunityTh2 Cells and mast cellsCDw125, 131Eosinophils, B-cellsB-cell proliferation and maturation, stimulates IgA and IgM production
IL-6Pro-inflammatoryTh Cells, macrophages, fibroblastsCD126, 130B-cells, plasma cellsB-cell differentiation
IL-7Adaptive immunityBM stromal cells, epithelial cellsCD127Stem cellsB and T cell growth factor
IL-8Pro-inflammatoryMacrophagesIL-8RNeutrophilsChemotaxis for neutrophils and T cells
IL-9Adaptive immunityT cellsIL-9R, CD132T cellGrowth and proliferation
IL-10Anti-inflammatoryT cells, B cells, macrophagesCDw210B cells, macrophagesInhibits cytokine production and mononuclear cell function
IL-11Pro-inflammatoryBM stromal cellsIL-11Ra, CD130B cellsDifferentiation, induces acute phase proteins
IL-12Anti-inflammatoryT cells, macrophages, monocytesCD212NK cells, macrophages, tumor cellsActivates NK cells, phagocyte cell activation, endotoxic shock, tumor cytotoxicity, cachexia
IL-17Pro-inflammatoryTh17 cellsIL-17RMonocytes, neutrophilsRecruits monocytes and neutrophils to the site of infection. Activation of IL-17 in turn activate downstream of many cytokines and chemokine, such as IL‐1, IL‐6, IL‐8, IL‐21, TNF‐β, and MCP‐1
IL-18Pro-inflammatoryMacrophages, dendritic cells, and epithelial cellsCD218a (IL-18Ra)Monocytes and T cellsRecruits monocytes and T lymphocytes. Synergist with IL-12 in the induction of IFN- γ production and inhibition of angiogenesis.
IL-22Anti-inflammatoryActivated T-cells and NK cellsIL-22RStromal and epithelial cellsStimulation of cell survival, proliferation
IL-37 (1L-1F7)Anti-inflammatoryB-cells, NK cells, and monocytesCD218a (IL-18Ra) and potentially SIGGRBelieved to act as a negative regulator inside the cell
where it interacts with SMAD3 that is activated downstream of TGFβ activity.
IL-38 (IL-1F10)Anti-inflammatoryB cells and macrophagesIL-1R1Unknown
IFN-αPro-inflammatoryMacrophages, neutrophils, and some somatic cellsCD118 (IFNAR1, IFNAR2)VariousAnti-viral
IFN-βPro-inflammatoryFibroblastsCD118 (IFNAR1, IFNAR2)VariousAnti-viral, anti-proliferative
IFN-γPro-inflammatoryT Cells and NK cellsCDw119 (IFNG R1)VariousAnti-viral, macrophage activation, increases neutrophil and monocyte function, MHC-I and -II expression on cells
M-CSFAdaptive immunityFibroblasts, endotheliumCD115Stem cellsMonocyte production and activation
TGF-βAnti-inflammatoryT cells and B cellsTGF-βR1, 2, 3Activated T and B cellsInhibits T and B cell proliferation, inhibits hematopoiesis, promote wound healing
TNF-αPro-inflammatoryMacrophagesCD120a,bMacrophagesPhagocyte cell activation, endotoxic shock
TNF-βPro-inflammatoryT CellsCD120a,bPhagocytes, tumor cellsChemotactic, phagocytosis, oncostatic, induces other cytokines
Abbreviations: IL; interleukin, TNF; tumor necrosis factor, IFN; interferon, G-CSF; granulocyte colony stimulating factor, GM-CSF; granulocyte macrophage colony stimulating factor, M-CSF; macrophage colony stimulating factor, TGF; transforming growth factor, CD; cluster of differentiation; CDw; cluster of differentiation designated by only one monoclonal antibody, BM; bone marrow, DC; dendritic cells


Role of pro-inflammatory cytokines in pathogenesis of viral infection

During viral infections, like SARS-CoV-2, RSV, Parvovirus B19, and Influenza, the level of the pro-inflammatory cytokines is elevated and decreased upon clearance of the virus [1, 5]. Influenza A and SARS-CoV-2 virus infections lead to high replication of the virus in respiratory epithelial cells. In addition, the infection itself mediates an aggressive inflammatory response that itself can cause damage of lung cells. This contributes to a high number of apoptotic cells that are phagocyted by resident macrophages. Upon phagocytosis, macrophages release pro-inflammatory cytokines that recruit other immune cells and cause acute inflammation in the lung tissues, provoking fever and enhanced fibrosis.

Apoptotic cells are also known to release pathogen associated molecular patterns (PAMP) and bind pattern recognition receptors (PRRs) which lead to the activation of TLR2, TLR3, or TLR4 [7, 8]. This binding increases levels of the local IL-1β and IL-8 and recruit macrophages and monocytes to remove the remaining fragments of the apoptotic cells, but simultaneously this will recruit other immune cells to the site of infection. Macrophages will present the viral peptides to T-helper cells that will activate and differentiate to produce Th1 pro-inflammatory cytokines associated with Th17 cell subsets. That in turn releases a wave of local IL-6, IFN-γ, MCP1, and IP-10 (CXCL10) into the circulation.

IL-12 and IL-8 are other cytokines that are produced to enhance the IFN-γ production which attracts monocytes and T lymphocytes but not neutrophils (in SARS-CoV-2), in order to induce apoptosis and eliminate the infected cells. The recruited cytotoxic T lymphocytes clear the infection and the immune response retreats to the haemostasis condition [2].

The regulatory T cells (Treg, CD4+, CD25+, Foxp3+ cell) are among T cells recruited to the site of infection. They are important mediators for immune regulation and control the level of cellular immune responses to the viral infections. Treg secretes IL-10, an important regulatory cytokine that inhibit the excessive T cells response and balance the immune response [8].


Pro-inflammatory cytokine regulation

As described above, a primary viral infection is associated with increased levels of Th1 pro-inflammatory cytokines, chemokines, and interferons. However, regulation of the cytokine secretion is crucial for keeping the haemostasis of the immune system. A misregulated cytokine production can lead to severe inflammation. An aberrant pro-inflammatory cytokine profile or a shift in the balance of the Th1/Th2 cytokine response has been suggested to play a role in the control of the viral infection and lead to viral persistence [Parvovirus]. Not only the expression but a balance in the kinetics of the pro-inflammatory and Th1/Th2 cytokine pattern is key to viral clearance and haemostasis of the immune system.

Several interleukins are involved in the regulation of the inflammation by suppressing the innate and acquired immunity. IL-10, IL-37, and IL-38 are among some which regulate the activation and proliferation of the T cells by binding to the inhibitory receptors, such as IL-18Ra (IL-R5) and IL-1R6. IL-38 is produced by B cells and macrophages and inhibits IL-1, IL-6, IL-17, IL- 22, and TNF [1, 11].

Misregulation of the immune response may lead to a massive increase of cytokine and chemokine levels which is referred to as cytokine release syndrome or cytokine storm. This phenomenon is characterized by an aggressive pro-inflammatory response in combination with an insufficient anti-inflammatory response, which results in the loss of homeostasis of the immune response [11].

Multiple causes can lead to a cytokine storm, which recently came into focus in medical research because it is believed to be a major cause for morbidity and mortality in SARS-CoV-2 infections. The SARS-CoV-2 virus may result in severe lung damage, which is caused not primarily by viral spreading but by overstimulation of the immune-system leading to a massive and uncontrollable inflammation [12].

Several pathologies involving a cytokine storm are described, like sepsis, toxic shock syndrome (TSS), macrophage activation syndrome (MAS), hemophagocytic lymphohistiocytosis (HLH), and malignancy associated syndrome of hyperinflammation (MASH) [14]. The key factors identified in pathologies involving a cytokine storm are TNF-α, interferons, IL-1β, MCP-1 (CCL2), and most importantly IL-6 [15]. Many more cytokines and chemokines play an important role in a cytokine storm, as summarized in the table Protein Biomarkers for Cytokine Release Syndrome in the ProcartaPlex Multiplex Cytokine Assay.

In the proposed pathogenesis of cytokine storm, activation of mainly T cells or lysis of immune cells induces a release of IFN-γ or TNF-α. This leads to the activation of macrophages, dendritic cells, other immune cells, and endothelial cells. After activation, these cells further release pro-inflammatory cytokines. Large amounts of IL-6 are produced by macrophages and endothelial cells, activating T cells and other immune cells and thereby creating a positive feedback-loop that results in a cytokine storm, inducing the release of many more cytokines and chemokines but also upregulating acute phase proteins.

References

  1. Turner MD (2014) Cytokines and chemokines: At the crossroads of cell signalling and inflammatory disease. Biochimica et Biophysica Acta 1843:2563–2582.
  2. Russell CD, Unger SA, Walton M, et. al. (2017) The Human Immune Response to Respiratory Syncytial Virus Infection. Clin Microbiol Rev, 30:481-502.
  3. Zlotnik A, Yoshie O (2012) The Chemokine Superfamily Revisited. Immunity, 36:705-16.
  4. Tay MZ, Poh CM, Renia L, et. al. (2020) The trinity of COVID-19: immunity, inflammation and intervention. Nat Rev Immunol, 28:1-12.
  5. Isa A (2006) Cytokine responses in acute and persistent human parvovirus B19 infection. Clin and Exp Immunol, 147: 419–425
  6. Skinner D, Marro BS, Lane TE (2019) Chemokine CXCL10 and Coronavirus-Induced Neurologic Disease. Viral Immunol. 32.
  7. Merad M (2020) Pathological inflammation in patients with COVID-19: a key role for monocytes and macrophages, Nat Rev Immunol, 6:1-8.
  8. Nelemans T, Kikkert M (2019) Viral Innate Immune Evasion and the Pathogenesis of Emerging RNA Virus Infections. Viruses, 11:961.
  9. D’Elia RV, Harrison K, Oyston PC, et. al. (2013) Targeting the “Cytokine Storm” for Therapeutic Benefit. Clin Vaccine Immunol, 20:319–327.
  10. Conti P, Ronconi G, Caraffa A, et. al.(2020) Induction of Pro-Inflammatory Cytokines (IL-1 and IL-6) and Lung Inflammation by Coronavirus-19 (COVI-19 or SARS-CoV-2): Anti-Inflammatory Strategies. J Biol Regul Homeost Agents, 34:327-331.
  11. Tisoncik JR, Korth MJ, Simmons CP, et. al. (2012) Into the Eye of the Cytokine Storm. Microbiol Mol Biol Rev, 76:16-32.
  12. Mehta P, McAuley DF, Brown M, Sanchez E, Tattersall RS, Manson JJ (2020) COVID-19: consider cytokine storm syndromes and immunosuppression. Lancet, 395:1033-1034.
  13. Shimabukuro-Vornhagen A, Gödel P, Subklewe M, et. al. (2018) Cytokine release syndrome. J Immunother Cancer, 6:56.
  14. Weaver LK, Behrens EM (2017) Weathering the storm: Improving therapeutic interventions for cytokine storm syndromes by targeting disease pathogenesis. Curr Treatm Opt Rheumatol, 3:33-48.
  15. Yiu HH, Graham AL, Stengel RF (2012) Dynamics of a cytokine storm. PLoS On,. 7:e45027.
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FAQs

What are the main pro-inflammatory cytokines? ›

The key pro-inflammatory cytokines are IL-1, IL-6, and TNF-α. These cytokines signal via type I cytokine receptors (CCR1) that are structurally divergent from other cytokine receptor types. They are crucial for coordinating cell mediated immune response and play a critical role in modulating the immune system.

What are proinflammatory and antiinflammatory cytokines? ›

Setting: Academic (university hospital). Results: Cytokines are regulators of host responses to infection, immune responses, inflammation, and trauma. Some cytokines act to make disease worse (proinflammatory), whereas others serve to reduce inflammation and promote healing (anti-inflammatory).

Why are pro-inflammatory cytokines important? ›

Inflammation is beneficial for pathogen clearance and protection against infection; therefore, pro-inflammatory cytokines are regulators of host responses to infection, inflammation, and trauma, which can also make disease worse in pathological conditions (1, 2).

What are proinflammatory chemokines? ›

Some chemokines are considered pro-inflammatory and can be induced during an immune response to recruit cells of the immune system to a site of infection, while others are considered homeostatic and are involved in controlling the migration of cells during normal processes of tissue maintenance or development.

Is CRP a proinflammatory cytokine? ›

During an inflammatory process in the body, the levels of C-reactive protein (CRP), a pro-inflammatory cytokine, rise dramatically. It has been suggested that testing CRP levels in the blood may be an additional way to assess cardiovascular disease risk.

Is TNF alpha a proinflammatory cytokine? ›

TNF-α, similarly to IL-6, is a proinflammatory cytokine, characterized by a broad spectrum of functions which also include cytotoxic and cytostatic effects against cancer cells [8]. TNF-α exerts an important influence on adipose tissue metabolism and function.

How many inflammatory cytokines are there? ›

There are two different types of inflammatory cytokines: Pro-inflammatory cytokines: Involved in inflammatory reactions (such as when tissues are damaged by bacteria, trauma, or any other cause)4. Anti-inflammatory cytokines: Regulate or control the pro-inflammatory cytokine response.

What is a proinflammatory effect? ›

Proinflammatory cytokines review

Proinflammatory cytokines are a general term for those immunoregulatory cytokines that favour inflammation. The net effect of an inflammatory response is determined by the balance between proinflammatory and anti-inflammatory cytokines.

Is TNF pro-inflammatory or anti-inflammatory? ›

The pro-inflammatory activities of tumour necrosis factor (TNF)-α are well established. This cytokine has been implicated in various autoimmune and inflammatory diseases such as rheumatoid arthritis, Crohn's disease, multiple sclerosis and uveitis.

What are the 5 cytokines? ›

Examine the five different types of cytokines found in the body: chemokines, interferons, interleukins, lymphokines, and tumor necrosis factor.

What are pro-inflammatory foods? ›

The pro-inflammatory foods are red meats, processed meats, organ meats (i.e. liver, kidney, brain, heart), non-oily fish (i.e. white fish), eggs, sugar-sweetened beverages (i.e. soda), tomatoes, and refined grains (bread or pasta and white rice).

What is the role of cytokines in the immune response? ›

Cytokines are small proteins that are crucial in controlling the growth and activity of other immune system cells and blood cells. When released, they signal the immune system to do its job. Cytokines affect the growth of all blood cells and other cells that help the body's immune and inflammation responses.

What are pro-inflammatory mediators? ›

Proinflammatory mediators are known to have a profound influence on the vasculature and cause increased vascular permeability, altered vascular morphogenic responses, leukocyte adhesion and transmigration, increased procoagulant activities, and increased platelet adhesion and aggregation.

What immune cells release cytokines? ›

Cytokines are mainly produced by macrophages and lymphocytes, although they can also be produced by polymorphonuclear leukocytes (PMN), endothelial and epithelial cells, adipocytes, and connective tissue. Cytokines are essential to the functions of macrophages.

What are pro-inflammatory cytokines and chemokines? ›

Cytokines are an exceptionally large and diverse group of pro- or anti-inflammatory factors that are grouped into families based upon their structural homology or that of their receptors. Chemokines are a group of secreted proteins within the cytokine family whose generic function is to induce cell migration [2, 3].

What kind of inflammation causes high CRP? ›

A wide variety of inflammatory conditions can cause elevated CRP levels, including : autoimmune conditions, including rheumatoid arthritis (RA), lupus, and certain types of inflammatory bowel disease (IBD), such as Crohn's disease and ulcerative colitis. pericarditis, which is inflammation of the lining of the heart.

What triggers CRP production? ›

C-reactive protein (CRP) is produced by the liver. The level of CRP rises when there is inflammation throughout the body. It is one of a group of proteins, called acute phase reactants, that go up in response to inflammation.

Why does CRP increase in inflammation? ›

Your liver releases more CRP into your bloodstream if you have inflammation in your body. High levels of CRP may mean you have a serious health condition that causes inflammation. Inflammation is your body's way of protecting your tissues and helping them heal from an injury, infection, or other disease.

What stimulates TNF? ›

Tumor Necrosis Factor-α (TNF-α)

Pro-inflammatory signaling pathways are stimulated by activation of either NF-κB or MAPK. A malicious link of TNF-α, inflammation, and cancer is well documented [82–84].

How does TNF cause inflammation? ›

TNF alpha does this by triggering the production of several immune system molecules, including interleukin-1 and interleukin-6. Both of these molecules are involved in a process that destroys cartilage and bone, driving even more inflammation and leading to the symptoms of many autoimmune diseases.

Is IL-6 proinflammatory cytokines? ›

IL-6 is an antiinflammatory cytokine required for controlling local or systemic acute inflammatory responses.

How do you measure proinflammatory cytokines? ›

Cytokines have been measured at messenger RNA (mRNA) levels using reverse transcription polymerase chain reaction (RT-PCR), and at protein levels by either cytokine bioassays or enzyme-linked immunosorbent assays (ELISA) [9].

How do you test for inflammatory cytokines? ›

Immunoassays: Immunoassays currently are the method of choice for determination of cytokines. Enzyme-linked immunosorbent assay (ELISA) is the commonly used form of immunoassay. ELISA uses a primary antibody for the capture and a secondary antibody conjugated to an enzyme or radioisotope for the detection.

Is IL 12 a proinflammatory cytokine? ›

IL-12 is a potent, pro-inflammatory cytokine produced by antigen presenting cells typically in response to microbial pathogens.

What protein causes inflammation in the body? ›

Research shows that what you eat can affect the levels of C-reactive protein (CRP)—a marker for inflammation—in your blood. That could be because some foods like processed sugars help release inflammatory messengers that can raise the risk of chronic inflammation.

How do you reduce inflammatory cytokines? ›

One of the most effective of these mechanisms is the role of physical activity in reducing the production of pro-inflammatory cytokines due to strengthening the immune system. Other mechanisms that can affect adipose tissue include reducing inflammation in the tissue and finally improving hypoxia.

What are pro inflammatory genes? ›

Proinflammatory genes are highly expressed in several metabolic disorders associated with obesity. But it is not clarified whether gene expression levels and downstream inflammatory markers are related to the metabolic state or the presence of obesity.

What is a proinflammatory state? ›

A proinflammatory state is related to atherosclerosis, and recent studies suggest that acute phase reactants correlate with circulating concentrations of homocysteine.

Is IL 4 a proinflammatory cytokine? ›

Results of this study indicate that IL-4 alone can act as a proinflammatory cytokine in the gut of normal mice, inducing a rapid onset and short-lived colonic injury while maintaining a Th2-type cytokine profile that functions via a local T cell-independent mechanism involving TNF-alpha.

Is interferon gamma a proinflammatory cytokine? ›

IFN-γ is a proinflammatory cytokine involved in Th1-driven immune responses.

What are the 6 groups of cytokines? ›

Cytokines include Interleukins, Lymphokines, Monokines, Interferons (IFN), colony stimulating factors (CSF), Chemokines and a variety of other proteins. Type-1 cytokines are cytokines produced by Th1 T-helper cells while Type-2 cytokines are those produced by Th2 T-helper cells.

What are 4 types of cytokines? ›

Different types of cytokines had been discovered, including chemokines, interferons (IFN), interleukins (IL), lymphokines and tumor necrosis factor (TNF) [1, 2, 3, 4].

What are the most important cytokines? ›

The major acute innate cytokines, IL-1, TNF-α, IL-6, IL-12, CXCL8 (formerly IL-18), G-CSF, and GM-CSF, are used locally to activate endothelial cells and local tissue leukocytes (mast cells [MCs], dendritic cells [DCs], γδ T cells, and neurones), triggering cytokine-mediated amplification loops generating chemokine ...

Are eggs pro-inflammatory? ›

For example, the cholesterol content of eggs has been reported to promote pro-inflammatory signaling by inducing cytotoxicity and stimulating the formation of lipid rafts in plasma membranes of leukocytes, which creates hypersensitivity to pro-inflammatory signaling.

Are bananas inflammatory? ›

Researchers found that not only did both types of bananas reduce inflammation, they also had an antioxidant effect, which helped keep immune cells functioning optimally.

Is coffee inflammatory? ›

Research suggests that coffee does not cause inflammation in most people—even if your norm is more than one or two caffeinated cups. In fact, it's quite the opposite. Coffee may have anti-inflammatory effects in the body.

What happens when too many cytokines are released? ›

Cytokines are part of a healthy immune system. These small proteins help control the growth and activity of your blood cells and immune cells. Cytokines tell your immune system to do its job. But when too many cytokines are released, it can cause your immune system to go into overdrive, resulting in cytokine storm.

What foods increase cytokines? ›

Sugar. It may be hard to resist desserts, pastries, chocolate bars, sodas, even fruit juices. However, the American Journal of Clinical Nutrition warns that processed sugars trigger the release of inflammatory messengers called cytokines.

Do mast cells release cytokines? ›

Mast cells synthesize and secrete histamine, proteases, prostaglandin D2, leukotrienes, heparin, and a variety of cytokines, many of which are implicated in CVD (36, 93–100). Furthermore, mast cells enhance endothelial inflammatory responses through upregulation of innate immune mechanisms (101, 102).

Which cytokine has some anti-inflammatory effects? ›

Major anti-inflammatory cytokines include interleukin (IL)-1 receptor antagonist, IL-4, IL-6, IL-10, IL-11, and IL-13. Specific cytokine receptors for IL-1, tumor necrosis factor-alpha, and IL-18 also function as proinflammatory cytokine inhibitors.

Is IL-12 anti-inflammatory? ›

IL-12 can aid in the activation and regulation of several cytotoxic immune cells including macrophages, natural killer cells, and T cells, thus making it a 'pro-inflammatory cytokine'.

What is a proinflammatory state? ›

A proinflammatory state is related to atherosclerosis, and recent studies suggest that acute phase reactants correlate with circulating concentrations of homocysteine.

What are the types of cytokines? ›

Different types of cytokines had been discovered, including chemokines, interferons (IFN), interleukins (IL), lymphokines and tumor necrosis factor (TNF) [1, 2, 3, 4].

How do you reduce inflammatory cytokines? ›

One of the most effective of these mechanisms is the role of physical activity in reducing the production of pro-inflammatory cytokines due to strengthening the immune system. Other mechanisms that can affect adipose tissue include reducing inflammation in the tissue and finally improving hypoxia.

Which foods are pro-inflammatory? ›

Foods with a higher pro-inflammatory potential are red meat, processed meat, and organ meat; refined carbohydrates such as white bread, white rice, and many desserts; and sweetened beverages including colas and sports drinks.

What are pro-inflammatory mediators? ›

Proinflammatory mediators are known to have a profound influence on the vasculature and cause increased vascular permeability, altered vascular morphogenic responses, leukocyte adhesion and transmigration, increased procoagulant activities, and increased platelet adhesion and aggregation.

Is IL-12 a proinflammatory cytokine? ›

IL-12 is a potent, pro-inflammatory cytokine produced by antigen presenting cells typically in response to microbial pathogens.

How do cytokines affect blood pressure? ›

Cytokines produced by the innate and adaptive immune systems contribute to the pathogenesis of hypertension by modulating renal function. Macrophages and T lymphocytes directly regulate BP and target organ damage. Dendritic cells and B cells can influence hypertensive responses by facilitating T-cell activation.

What are the 5 classic signs of inflammation? ›

Based on visual observation, the ancients characterised inflammation by five cardinal signs, namely redness (rubor), swelling (tumour), heat (calor; only applicable to the body' extremities), pain (dolor) and loss of function (functio laesa).

What are pro inflammatory genes? ›

Proinflammatory genes are highly expressed in several metabolic disorders associated with obesity. But it is not clarified whether gene expression levels and downstream inflammatory markers are related to the metabolic state or the presence of obesity.

How do inflammatory cytokines work? ›

Function. Inflammatory cytokines play a role in initiating the inflammatory response and to regulate the host defence against pathogens mediating the innate immune response. Some inflammatory cytokines have additional roles such as acting as growth factors.

What are the most important cytokines? ›

The major acute innate cytokines, IL-1, TNF-α, IL-6, IL-12, CXCL8 (formerly IL-18), G-CSF, and GM-CSF, are used locally to activate endothelial cells and local tissue leukocytes (mast cells [MCs], dendritic cells [DCs], γδ T cells, and neurones), triggering cytokine-mediated amplification loops generating chemokine ...

What are the four functions of cytokines? ›

Cytokines have important roles in chemically induced tissue damage repair, in cancer development and progression, in the control of cell replication and apoptosis, and in the modulation of immune reactions such as sensitization.

What immune cells release cytokines? ›

Cytokines are mainly produced by macrophages and lymphocytes, although they can also be produced by polymorphonuclear leukocytes (PMN), endothelial and epithelial cells, adipocytes, and connective tissue. Cytokines are essential to the functions of macrophages.

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