As far as I understand, bacteria cannot produce cytokines such as interleukins. However, I have not read an explanation as to why they cannot. Perhaps it has to do with an evolutionary limitation. Yet, if this is the case, why would bacteria be incapable of acquiring new functions such as cytokine production during their evolution, especially intracellular bacteria which reside within immune cells. If bacteria have not been able to acquire this function, then maybe it has to do with a biological constraint (size of the proteins, amino acid composition, machinery or bioenergetic capacity). If anyone knows the exact reason or has a knowledgeable explanation I would really like to read it. Thanks.
It seems especially pertinent to point out from the start that many cytokines are anti-inflammatory/immunosuppressive. The immune system has evolved to remove pathogens from the body, and normally these cytokines act to deactivate the immune response once an infection has been cleared. It should not be surprising that pathogens have co-evolved defences to the immune system, including interference with cytokine networks and even production of anti-inflammatory cytokine homologs, ostensibly to subvert the immune response. Below are but a few examples of this.
Many viruses exploit the strategy of using homologs of cellular cytokines or cytokine receptors to shield virus-infected cells from immune defenses and enhance virus survival in the host. The presence of virus-encoded homologs of cellular proteins may be an indicator of the importance of these cellular components in immune mechanisms for combating this virus in vivo. A number of herpes viruses harbor homologs of IL-10. Epstein–Barr virus (EBV)-encoded IL-10 (ebvIL-10), the first viral homolog of IL-10 identified, shares many but not all of the biological activities of cellular IL-10 and may play an important role in the host-virus interaction. In addition to EBV, another virus, the Orf poxvirus (OV), which can infect humans, has its own IL-10 homolog, ovIL-10.
IL-10 has several immunosuppressive activities that would be favorable for CMV, such as down-regulation of MHC class I and II expression, inhibition of production of inflammatory cytokines, and interference with antigen presentation. Murine CMV infection induces transient early expression of IL-10, which plays an essential role in MHC class II down-regulation. EBV infection causes expression not only of ebvIL-10, but also of human IL-10. We demonstrated here that human CMV encodes its own functional IL-10 homolog, which is expressed by CMV-infected cells. Thus, it seems likely that herpes viruses acquire many advantages by using IL-10-specific biological activities either of virus-encoded or host IL-10s.
Another intriguing aspect in the parasite relationship is the fact that parasites could release factors that mimic host cytokines. For instance, (1) hydatid ﬂuid fractions mimicked IL-1, IL-2, and IL-6; (2) an IFN-γ homolog that binds to the IFN-γ receptor and induced change in lymphoid cells has been identiﬁed in an intestinal nematode; (3) two homologs of the human macrophage migration inhibitory factor (MIF) have been characterized in the human parasitic nematode Brugia malayi and termed Bm-MIF-1 and Bm-MIF-2, both having functional properties similar to the MIF human counterpart; (4) Toxoplasma gondii releases cyclophilin-18 (C-18) that signals through the chemokine receptor CCR5 leading to the IL-12 synthesis by dendritic cells and a strong protective response; (5) the tapeworm Hymenolepis diminuta has been shown to express an IL-12-like peptide, one of the suggested hypothesis being that the peptide could act as a competitive antagonist for the IL-12 receptor, thus contributing to the general immunosuppression.
I have not found such explicit examples of bacteria producing cytokine homologs. However, their ability to produce immune modulating, paracrine signalling proteins, which is essentially the definition of a cytokine, is well known. The following reviews are quite extensive and provides numerous examples:
In recent years it has become apparent that bacteria produce many molecules which have profound effects on the capacity of leukocytes and tissue cells to produce selected cytokine networks. Thus attention will have to switch from the current view of the host cell as the only controlling factor in cytokine biology, once the bacterium has stimulated this cell, to one in which the bacterium, by modifying its exported or structural molecules or by direct interaction with the cell, can directly modify cytokine networks.
Recent cytokine transgenic knockouts demonstrate that the normal benign response to commensal gut microflora becomes a lethal inflammatory state in the absence of the cytokines interleukin 2 or interleukin 10... We propose that the ability of the multicellular organism to live harmoniously with its commensal microflora must depend on mutual signalling involving eukaryotic cytokines and prokaryotic cytokine-like molecules. Such interactive signalling sets up non-inflammatory cytokine networks in tissues which form the background on which responses to infectious microorganisms must be built and related... It is now clear that bacteria contain and produce a large number of diverse molecules which can selectively induce the synthesis of both pro-inflammatory and immunomodulatory/anti-inflammatory cytokines.
Finally, the mechanisms by which bacteria can co-evolve such cytokine-like molecules is discussed in this review:
Recent studies have begun to reveal that many bacterial pathogens mimic the function of host proteins to manipulate host physiology and cellular functions for the microbe's benefit. This is in contrast with the strategies used by some pathogens that involve microbial products with activities lacking clear counterparts in eukaryotic cells. Here we consider recent structural work that provides unique insights into the mechanisms of host mimicry by bacterial virulence factors. In some cases, these factors are homologues of host proteins that have been incorporated into the genome of the pathogen and subverted for its benefit. In others, convergent evolution has produced new effectors that have no obvious relationship to host factors. However, although hidden at the sequence level, the determination of the crystal structures of several bacterial factors and bacterial–host protein complexes has revealed the presence of mimicry at the molecular level.
Bacteria don't produce cytokines naturally (while some might be 'useful' for immune suppression, bacteria can't use human genes/DNA, which has introns, and the chance to randomly come up with a gene that makes the correct protein would be astronomically low).
However, bacteria CAN produce cytokines, if they are engineered to so: here is a company that sells various cytokines, many of which they produce in E. coli. To make this work the company had to remove all introns from the cytokine producing genes and add a bacterial promoter to the gene.
The only thing, which is needed for some human molecules to work (e.g. antibodies), that bacteria can not produce (at least with current technology), are glycosylations of proteins. I checked it quickly and it doesn't look like cytokines are glycosylated (at least in principal, there are very likely some exceptions).