After 24 hr ESAT-6 1 <i>μ</i>g/ml stimulation, the percentage of IL-1b-expressed hMDM was borderline lower in the active TB patients (<i>n</i> = 9) than in the LTBI cases (<i>n</i> = 10) (14.0 ± 11.2% vs. 31.6 ± 22.5%, <i>P</i> = 0.065).
Although Rv1813c is not required for survival of M. tuberculosis in vitro, including under conditions in which MprAB and DosRST signaling are activated, an M. tuberculosis ΔRv1813c mutant is attenuated in the low-dose aerosol model of murine tuberculosis, where it exhibits a lower bacterial burden, delayed time to death, and decreased ability to stimulate proinflammatory cytokines interleukin-1β (IL-1β) and IL-12.
Following multivariate analyses adjusting for covariates IL6, interleukin 1β (IL1β), and interleukin 1Rα (IL1Rα) were associated with increased risk and IFNβ with decreased TB risk.
From a wealth of rodent studies using live infection models, the following conclusions can be drawn: (1) neutralization or gene deletion for TNF-alpha is frequently associated with reduction of host defense in models of live Gram-positive or Gram-negative infections as well as infection by intracellular microbes such as Salmonella and Listeria; (2) absence of the IL-1 receptor can also result in decreased resistance to Listeria or Gram-positive bacteria and (3) TNF-alpha and IFN-gamma are required for defense against infection caused by Mycobacterium tuberculosis.
HHC with CC (P < 0.03, OR = 1.833 and 95% CI = 1.1-3.35) genotype in IL-1β and GA (P < 0.0001, OR = 4.612 and 95% CI = 2.225-9.702) genotype in IL-10 were at increased risk of developing tuberculosis.
Impairment in TNF, IL-1β, and IL-17 production upon stimulation with mycobacterial antigens may contribute to the increased susceptibility to M. tuberculosis infection observed in HTLV-1 infected individuals.
Interleukin-37 (IL-37), a novel member of the IL-1 family, plays fundamental immunosuppressive roles by broadly reducing both innate inflammation and acquired immunity, but whether it is involved in the pathogenesis of tuberculosis (TB) has not been clearly elucidated.
Most of the host components involved in TB inflammation, including cytokines (interferons, interleukin (IL)-1, IL-10, tumour necrosis factor) and cells (neutrophils, macrophages, regulatory T cells, type 1 helper lymphocytes, pneumocytes), exhibit dual features: they foster or repress local inflammatory events.
Our results with CLEC9A-knocked down cells and a CLEC9A-Fc fusion protein as blocking agents show that CLEC9A is involved in the activation of SYK and MAPK signaling in response to heat-killed M. tuberculosis H37Ra treatment, and it then promotes the production of CXCL8 and IL-1β in macrophages.