I am in a big confusion about the pro and anti-inflammatory cytokines. One of my colleagues screened various probiotic bacteria on cytokine profile and based on these they are classifying their bacteria into good and bad for anti-inflammatory studies. Is this the correct way to screen? When I read literature there is lot of contradiction to decide the cytokine is inflammatory and anti-inflammatory. So, I request you all to help me in this regard. Thanks for your concern in-advance.
Might help!
J Endocrinol. 2008 Apr;197(1):139-50. doi: 10.1677/JOE-07-0638.
Interaction between pro-inflammatory and anti-inflammatory cytokines in insulin-producing cells.
There is not a real way to divide cytokines in good or bad. In fact even if there are cytokines that are mainly pro-inflammatory, the final effect depends mainly on the pathology on what you want to work!
As Paola says, it has a lot to do with context. IL-22 for example is thought to be anti-inflammatory or protective in the gut but may be pro inflammatory or detrimental in the skin. IFN gamma is generally thought to be pro inflammatory but its absence could result in uncontrolled infection. Look at the disease process that you hope to influence with probiotics and see which cytokines drive this process. In this context these are your pro inflammatory or perhaps, disease-driving cytokines.
Generally, cytokines that inhibit inflammatory T cell (Th1) differentiation such as IL-10, TGB beta are anti-inflammatory CKs. This definition because activated Th1 cell secretes IFN gamma that activates other leukocytes as NKCs, APCs, that when activated release TNF alfa, IL-1 what are called inflammatory CKS.
it is true that some cytokines can be either inflammatory or anti inflammatory depending on context, but others such as Il1B and TNF alpha will always be inflammatory. And I could probably find ones too that are also always anti inflammatory so I like Hesham's answer too.
For general screening IL-6, IL-1beta and TNF-alpha they are considered as inflammatory cytokines where as IL-10, IL-17 and TGB-beta are anti-inflammatory. Some how their specificity for diseases is also a point of concern.
Lots of good responses here. Clearly in some contexts (specific cytokines and specific receptors) cytokines can be broadly pro- or anti-inflammatory but it is more complex than this: cytokines can elicit different highly specialised events in different cell types. In some respects it is useful to categorise cytokines as broadly pro-or anti-inflammatory, after all TNF overexpression has a profound effect in driving rheumatoid arthritis and other inflammatory diseases and IL-10 knockout mice spontaneously deliver colitis but bear in mind that even in the case of TNF it has two different receptors (TNFR1(p55) and TNFR2(p75)) and while TNFR1 signals pro-inflammatory events, TNFR2 is now thought to signal anti-inflammatory events. This is why TNFR1 blockade has been suggested as an alternative possibly better therapy than TNF biologics for the therapy of chronic inflammatory diseases.
Cytokines (CK) are classified according to their role in inflammation.
· Anti-inflammatory CKs: IL-4, IL-13, IL-10
· Pro-inflammatory CKs : TNF, IL-1, IL-12, IL-15
· Ambivalent CKs: IFNγ, TGKβ, IL-6
The classification is not absolute :
1. CK can be pro or anti-inflammatory at different stages of the inflammatory reaction.
2. CK have antagonists and agonists that suppress or promote their function.
3. CK must bind to specific receptors to activate the target cell.
These receptors are soluble or expressed on membrane of cells .
Soluble receptors can be agonists (for IL-6) or antagonists (for TNF)
4. The inflammatory response depends on:
- Balance between pro and anti-inflammatory CK
- Balance between CK and its natural inhibitor (comparable to acid-base equilibrium)
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