Disease relevance of IL10

• Expression of interleukin-10 and suppressor of cytokine signaling-3 associated with susceptibility of cattle to infection with Mycobacterium avium subsp paratuberculosis [1].
• Therefore, the combination of inherent resistance to intracellular degradation and suppression of macrophage activation through oversecretion of IL-10 may contribute to the virulence of M. avium subsp. paratuberculosis in cattle [2].
• IL-10 mRNA was detected in cells from the milk of 2 mastitic cows and 1 normal cow, and IL-12 mRNA was detected in 2 cows with mastitis [3].
• Although IL-1beta, IL-6 and IL-10 mRNAs were barely detectable in fresh B cells from cows with persistent lymphocytosis, transcripts encoding these cytokines were strongly and rapidly upregulated in B cells after cell culture [4].
• Together, the data suggests that IL-10 and IFN-gamma are critical molecules involved in the response to this intraerythrocytic protozoan infection [5].

High impact information on IL10

• The inhibitory effect of IL-10 on BLV expression depends on soluble factors secreted by macrophages [6].
• Type 1 cytokines (interleukin-2 [IL-2], IL-12, and gamma interferon) increase in freshly isolated peripheral blood mononuclear cells (PBMCs) of animals with an early disease stage of bovine leukemia virus (BLV) infection, while IL-10 increases in animals with a late disease stage [6].
• Although IL-10 has an immunosuppressive role in the host immune system, IL-10 also inhibits BLV tax and pol mRNA levels in vitro [6].
• The present study, combined with our previous findings, suggests that increased IL-10 production in late disease stages suppresses BLV mRNA levels, while IL-2-activated immune responses stimulate BLV expression by BLV-infected B cells [7].
• In contrast, IL-10 increased with disease progression [7].

Biological context of IL10

• Nonetheless, analysis of a CD4+ T cell clone before and after transformation with the parasite indicated that infection does alter the pattern of cytokine expression, with apparent upregulation of IL10 [8].
• Only IL-10 gene expression was consistently enhanced by M. avium subsp. paratuberculosis stimulation of PBMCs from subclinically infected cattle [9].
• Agents that prevented the acquisition of bacteriostatic activity by activated macrophages also prevented the induction of apoptosis in infected macrophages (IL-10 and neutralizing anti-TNF-alpha) [10].
• Downregulation of these same cytokine messages as well as IFN-gamma message occurred within a 20-h period when IL-10 was added exogenously to cultures of total leukocytes [11].
• Evaluation of TNF-alpha, IL-8 and IL-10 transcriptional activity in milk from healthy dairy cows during lactation period [12].

Anatomical context of IL10

• CONCLUSIONS AND CLINICAL RELEVANCE: Monocytes obtained from cows with subclinical infection with MAP had upregulated expression of IL-10 and SOCS-3 within the first 2 hours after exposure to MAP organisms [1].
• When cytokine expression by macrophages incubated with M. avium subsp. paratuberculosis was compared to those of macrophages incubated with M. avium subsp. avium, M. avium subsp. paratuberculosis-infected cells showed greater expression of IL-10 (6 and 24 h) and less expression of TNF-alpha (6 h) [2].
• An increase in the transcription of IL-10 and transforming growth factor beta (TGF-beta) genes in SEC1-stimulated cultures was attributed to the CD4(+) CD25(+) T-cell subpopulation [13].
• In vitro infection with Theileria parva is associated with IL10 expression in all bovine lymphocyte lineages [8].
• Analysis of cytokine mRNA indicates that bovine B cells constitutively express tumour necrosis factor-alpha (TNF-alpha) and interleukin (IL)-1beta transcripts in vitro, while IL-10 mRNA expression is induced following sIgM cross-linking [14].

Associations of IL10 with chemical compounds

• Chemical inhibition of the MAPK(p38) signaling pathway (SB203580) resulted in decreased expression of IL-10 and increased expression of IL-12 at 6h post-infection [15].
• The cells also expressed cytokine transcripts, namely, those of IL-12, IFN-gamma and TNF-alpha, but not IL-2, IL-4, IL-6, IL-7 and IL-10 [16].
• Production of IL-10 was also evident following culture with CD40L+ cells or lipopolysaccharide primarily by the SIRPalpha+ CC81Ag- DC [17].

Other interactions of IL10

• RESULTS: Monocytes from infected cows had greater expression of IL-10 and SOCS-3 at 2 hours of coincubation with MAP and lower expression of TNF-alpha and IL-12 when results for all incubation times were combined [1].
• In this report, mRNA expression of interferon (IFN)-gamma and interleukin (IL)-2 (type 1 cytokines), and of IL-4 and IL-10 (type 2 cytokines) were evaluated in concanavalin A-stimulated peripheral blood mononuclear cells (PBMC) from BLV-infected sheep [18].
• Within 32 h of challenge, increased levels of IL-8, TNF-alpha, IL-10, and IL-12 were detected, however, the elevated levels of these cytokines were not sustained for longer than a 24h period [19].
• In particular, S. uberis infection was characterized by the sustained elevation of higher milk levels of IL-1 beta, IL-10, IL-12, IFN-gamma, and C5a, relative to S. marcescens infection [20].
• The results showed that the cell lines transcribed message for IFNgamma, TNFalpha, IL-4 and IL-10 whereas no mRNA for IL-2 or IL-1beta was detected [21].

Analytical, diagnostic and therapeutic context of IL10

• In addition, using RT-PCR with peripheral blood leukocytes and spleen leukocytes, the Griess reaction, and a killing assay, we provide evidence for the importance of iNOS in a successful immune response to B. bovis infection and for high and persistent IL-10 mRNA expression when the immune response is unsuccessful [5].
• Optimal conditions were then used to deliver increasing amounts of IL-10 plasmid intra-articularly (i.a.) in the collagen-induced arthritis (CIA) mouse model [22].
• No consistent differences were seen in any of the cell populations when the samples were analyzed for IL-10 and levels of mRNA for IL-2 and IL-4 were low and highly variable in both infected and control groups in all 3 lymphocyte populations [23].

References