The Lung Immune Niche in Tuberculosis: Insights from Studies on Human Alveolar Macrophages

Abstract

Tuberculosis (TB) is a disease that continues to cause global mortality and morbidity. Transmission of Mycobacterium tuberculosis (Mtb) occurs by aerosol transmission from an infected case, making the lung the primary portal of entry for the bacterium. Alveolar macrophages are the frontline cells involved in the control of subsequent replication and spread of disease. Although animal models have provided important information in the field of macrophage immunology and cell biology, human TB disease has several unique features. Therefore, an understanding of human alveolar macrophage biology and their interactions with Mtb is important, not only to understand how to address TB control at various stages of the disease but also to develop optimal future vaccination and drug strategies. Despite limitations of human sample access, technical expertise in cell processing, and access to reagents, significant advances have been made in the field providing critical insights into host-pathogen interactions This review describes the unique features and the immune responses of human alveolar macrophages in the context TB infection.

Impact of Demographic Characteristics and Therapy on Tuberculosis Incident Cases

“…Such a suggestion has been made based on the variability in the interaction of the Mycobacterium tuberculosis inside the immune system. Likewise, previous studies indicated that the Mycobacterium tuberculosis has often interacted with many types of cytokines to infect the lungs of its host [67,73,74]. Thus, the interaction of Mycobacterium tuberculosis has involved several types of cytokines while causing TB within the lungs of an infected person or animal.…”

“…The Mycobacterium tuberculosis agent has disabled the alveolar macrophage to infect the lungs of its host. Research indicated that the macrophage is an antigen that has engulfed or killed the foreign particles attempting to invade the immune system of a host [67,68,59]. However, in many instances, the Mycobacterium tuberculosis species has been observed in inhibiting the function of T-lymphocytes and immune response of the alveolar macrophages to survive within a TB-infected person or animal [68,69,59].…”

“…Depending on its strain, the Mycobacterium tuberculosis species have behaved differently with specific types of cytokines. The H37Rv strain of Mycobacterium tuberculosis, for instance, might inhibit the macrophages from secreting tumor necrosis factor (TNF) and interleukin-12 (IL-12) cytokines that may have prevented it from invading the immune system of a host Olsen, et al (2016) [67,75] The dysfunction of macrophages is critical for the survival of Mycobacterium tuberculosis inside the host. Similarly, research indicated that such an action of the H37Rv strain has often sustained the Mycobacterium tuberculosis agent in obliterating the production of TNF and nitric oxide in its favor to survive, grow, and transform into pulmonary tuberculosis within the immune system of such a host Olsen, et al (2016) [67,75,74] The K-strain of the Mycobacterium tuberculosis, on the contrary, has interacted with different kinds of cytokines within the immune system of the host.…”

Mycobacterium tuberculosis and host interactions in the manifestation of tuberculosis

“…Human alveolar macrophages are the frontline cells controlling TB's subsequent replication and spread of infection. Therefore, understanding the alveolar macrophage biology as an immune response and their interactions with M.tb is essential for understanding how to address TB control at various stages of the disease and developing better future vaccination and drug strategies [88] .…”