Interleukin 22 Inhibits Intracellular Growth of Mycobacterium tuberculosis by Enhancing Calgranulin A Expression

Dhiman, Rohan; Venkatasubramanian, Sambasivan; Paidipally, Padmaja; Barnes, Peter F.; Tvinnereim, Amy; Vankayalapati, Ramakrishna

doi:10.1093/infdis/jit495

Cited by 60 publications

(59 citation statements)

References 52 publications

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“…IL-22-producing cells at mucosal surfaces play a crucial role in the host innate defense against microorganisms, including M.tb (Aujla and Kolls, 2009). A recent report showed that IL-22 can inhibit the growth of M.tb in macrophages by enhancing phagolysosomal fusion (Dhiman et al, 2014). In addition, the IL-22-producing T cell-mediated immunity is important for the protective anti- M.tb response (Bhuju et al, 2012).…”

Section: Discussionmentioning

confidence: 99%

SIV Infection Facilitates Mycobacterium tuberculosis Infection of Rhesus Macaques

et al. 2017

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Tuberculosis (TB) is a common opportunistic infection and the leading cause of death for human immunodeficiency virus (HIV)-infected patients. Thus, it is necessary to understand the pathogenetic interactions between M.tb and HIV infection. In this study, we examined M.tb and/or simian immunodeficiency virus (SIV) infection of Chinese rhesus macaques. While there was little evidence that M.tb enhanced SIV infection of macaques, SIV could facilitate M.tb infection as demonstrated by X-rays, pathological and microbiological findings. Chest X-rays showed that co-infected animals had disseminated lesions in both left and right lungs, while M.tb mono-infected animals displayed the lesions only in right lungs. Necropsy of co-infected animals revealed a disseminated M.tb infection not only in the lungs but also in the extrapulmonary organs including spleen, pancreas, liver, kidney, and heart. The bacterial counts in the lungs, the bronchial lymph nodes, and the extrapulmonary organs of co-infected animals were significantly higher than those of M.tb mono-infected animals. The mechanistic studies demonstrated that two of three co-infected animals had lower levels of M.tb specific IFN-γ and IL-22 in PBMCs than M.tb mono-infected animals. These findings suggest that Chinese rhesus macaque is a suitable and alternative non-human primate model for SIV/M.tb coinfection studies. The impairment of the specific anti-TB immunity is likely to be a contributor of SIV-mediated enhancement M.tb infection.

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Section: Discussionmentioning

confidence: 99%

SIV Infection Facilitates Mycobacterium tuberculosis Infection of Rhesus Macaques

et al. 2017

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“…In another side, S100A8/A9 (calprotectin) was discovered as an immunogenic protein expressed by neutrophils with potent anti‐microbial properties . Reports showed that IL‐22 inhibits intracellular growth of mycobacterium tuberculosis, and contributes to antimicrobial defense and restitution of colonic epithelial integrity during colitis by enhancing S100A8 expression . There is also accumulating evidence that S100A8/A9 not only act as biomarkers for numerous inflammatory diseases, but are also proposed as biomarkers for other cancers, such as prostate, breast and colorectal .…”

Section: Discussionmentioning

confidence: 99%

Inflammation‐induced S100A8 activates Id3 and promotes colorectal tumorigenesis

Zhang

et al. 2015

Intl Journal of Cancer

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The aberrant expression of S100A8 and S100A9 is linked to nonresolving inflammation and ultimately to carcinogenesis, whereas the underlying mechanism that allows inflammation to progress to specific cancer types remains unknown. Here, we report that S100A8 was induced by inflammation and then promoted colorectal tumorigenesis downstream by activating Id3 (inhibitor of differentiation 3). Using gene expression profiling and immunohistochemistry, we found that both S100A8 and S100A9 were upregulated in the chemically-induced colitis-associated cancer mouse model and in human colorectal cancer specimens. Furthermore, we showed that S100A8 and S100A9 acted as chemoattractant proteins by recruiting macrophages, promoting the proliferation and invasion of colon cancer cell, as well as spurring the cycle that culminates in the acceleration of cancer metastasis in a nude mouse model. S100A8 regulated colon cancer cell cycle and proliferation by inducing Id3 expression while inhibiting p21. Id3 expression was regulated by Smad5, which was directly phosphorylated by Akt1. Our study revealed a novel mechanism in which inflammation-induced S100A8 promoted colorectal tumorigenesis by acting upstream to activate the Akt1-Smad5-Id3 axis.

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“…Furthermore, in non-human primate infected with Mtb, CD4 + T cells expressing membrane-bound IL-22 limit Mtb intracellular growth in macrophages (255). IL-22 can also inhibit intracellular growth of Mtb in human monocyte-derived macrophages by promoting phagolysosomal fusion and induction of Calgranulin A, a heterodimer of S100A8 and S100A9 proteins (256). Moreover, human NK cells cultured with Mtb-infected macrophages produce IL-22 and mediate macrophage activation (257).…”

Section: Cytokinesmentioning

confidence: 99%

Cytokines and Chemokines inMycobacterium tuberculosisInfection

et al. 2016

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Chemokines and cytokines are critical for initiating and coordinating the organized and sequential recruitment and activation of cells into Mycobacterium tuberculosis -infected lungs. Correct mononuclear cellular recruitment and localization are essential to ensure control of bacterial growth without the development of diffuse and damaging granulocytic inflammation. An important block to our understanding of TB pathogenesis lies in dissecting the critical aspects of the cytokine/chemokine interplay in light of the conditional role these molecules play throughout infection and disease development. Much of the data highlighted in this review appears at first glance to be contradictory, but it is the balance between the cytokines and chemokines that is critical, and the “goldilocks” (not too much and not too little) phenomenon is paramount in any discussion of the role of these molecules in TB. Determination of how the key chemokines/cytokines and their receptors are balanced and how the loss of that balance can promote disease is vital to understanding TB pathogenesis and to identifying novel therapies for effective eradication of this disease.

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Interleukin 22 Inhibits Intracellular Growth of Mycobacterium tuberculosis by Enhancing Calgranulin A Expression

Cited by 60 publications

References 52 publications

SIV Infection Facilitates Mycobacterium tuberculosis Infection of Rhesus Macaques

SIV Infection Facilitates Mycobacterium tuberculosis Infection of Rhesus Macaques

Inflammation‐induced S100A8 activates Id3 and promotes colorectal tumorigenesis

Cytokines and Chemokines inMycobacterium tuberculosisInfection

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