Joshua T. Mattila, PhD

  • Assistant Professor, Infectious Diseases and Microbiology, School of Public Health

Education & Training

  • Postdoc, University of Pittsburgh School of Medicine
  • PhD in Entomology, University of Minnesota, 2006
  • BS in Biology, Bemidji State University, 1996

Research Interests

Much of the world's population has been exposed to or is infected with Mycobacterium tuberculosis, the bacterium that causes tuberculosis (TB). TB is characterized by formation of structures called granulomas that are a mechanism for containing the bacteria but also serve as an intra-host niche for bacterial persistence. These two outcomes are mediated by a complex community of immune cells that need to work together to kill intracellular and extracellular Mtb while minimizing damage to the host. My lab’s primary focus is on identifying interactions between M. tuberculosis and the host at the granuloma level with an emphasis on identifying interactions between macrophages, neutrophils, and T cells that lead to protection or pathology. We have ongoing projects in several areas including studies on the role that myeloid-derived suppressor cells play in TB, type 1 and type 3 interferon function in TB, and identification of macrophage responses to HIV infection that contribute to poor outcomes in HIV/M. tuberculosis co-infection. We are also working on immunometabolism in TB to identify host and bacterial pathways that contribute to host-mediated antibacterial activity and bacterial persistence. In addition to out wet-lab projects, we collaborate with computational modelers where we test hypotheses in silico that cannot be easily tested in vivo or in vitro. Our long-term objective is to identify host-directed therapies that can improve and shorten the therapeutic regimens for TB treatment.


Talukdar P, Junecko BF, Lane DS, Maiello P and Mattila JT. 2022. Macrophages and neutrophils express IFNλs in granulomas from Mycobacterium tuberculosis-infected nonhuman primates. Front Immunol. 13: 985405. doi: 10.3389/fimmu.2022.985405. eCollection. PubMed PMID: 36189279; PubMed Central PMCID: PMC9516334.

Gideon HP, Hughes TK, Tzouanas CN, Wadsworth MH 2nd, Tu AA, Gierahn TM, Peters JM, Hopkins FF, Wei JR, Kummerlowe C, Grant NL, Nargan K, Phuah JY, Borish HJ, Maiello P, White AG, Winchell CG, Nyquist SK, Ganchua SKC, Myers A, Patel KV, Ameel CL, Cochran CT, Ibrahim S, Tomko JA, Frye LJ, Rosenberg JM, Shih A, Chao M, Klein E, Scanga CA, Ordovas-Montanes J, Berger B, Mattila JT, Madansein R, Love JC, Lin PL, Leslie A, Behar SM, Bryson B, Flynn JL, Fortune SM, Shalek AK. 2022. Multimodal profiling of lung granulomas in macaques reveals cellular correlates of tuberculosis control. Immunity. 55: 827-846.e10. doi: 10.1016/j.immuni.2022.04.004. Epub 2022 Apr 27. PubMed PMID: 35483355; PubMed Central PMCID: PMC9122264.

Mattila JT, Maiello P, Sun T, Via LE, Flynn JL. 2015. Granzyme B-expressing neutrophils correlate with bacterial load in granulomas from Mycobacterium tuberculosis-infected cynomolgus macaques. Cell Microbiol. 7: 1085-97. doi: 10.1111/cmi.12428. Epub 2015 Mar 12. PubMed PMID: 25653138; PubMed Central PMCID: PMC4570831.

Mattila JT, Ojo OO, Kepka-Lenhart D, Marino S, Kim JH, Eum SY, Via LE, Barry CE 3rd, Klein E, Kirschner DE, Morris SM Jr, Lin PL, Flynn JL. 2013. Microenvironments in tuberculous granulomas are delineated by distinct populations of macrophage subsets and expression of nitric oxide synthase and arginase isoforms. J Immunol. 191: 773-84. doi: 10.4049/jimmunol.1300113. Epub 2013 Jun 7. PubMed PMID: 23749634; PubMed Central PMCID: PMC3746594.

Mattila JT, Diedrich CR, Lin PL, Phuah J, Flynn JL. 2011. Simian immunodeficiency virus-induced changes in T cell cytokine responses in cynomolgus macaques with latent Mycobacterium tuberculosis infection are associated with timing of reactivation. J Immunol. 186: 3527-3537. doi: 10.4049/jimmunol.1003773. Epub 2011 Feb 11. PubMed PMID: 21317393; PubMed Central PMCID: PMC3311978.

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