Host–Pathogen Interactions in Tuberculosis

Espitia, Clara; Rodriguez, E; Ramón‐Luing, Lucero A.; Echeverría-Valencia, Gabriela; Vallecillo, Antonio J.

doi:10.5772/30310

Cited by 8 publications

(13 citation statements)

References 166 publications

(130 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…It has been established that mycobacteria have evolved a wide range of molecules, known as adhesions, to enable binding with fibronectin, a protein of the host extracellular matrix, and type I collagen fibers and, eventually, to invade host cells [ 34 ]. The cytoskeletal filamentous proteins actin and vimentin are responsible for cell migration, attachment to the substrate, maintaining cell shape, integrity of the cytoplasm, phagocytosis of bacterial agents, and elimination of intracellular pathogens [ 34 ].…”

Section: Resultsmentioning

confidence: 99%

Differences betweenMycobacterium-Host Cell Relationships in Latent Tuberculous Infection of MiceEx Vivoand Mycobacterial Infection of Mouse CellsIn Vitro

Ufimtseva

2016

Journal of Immunology Research

View full text Add to dashboard Cite

The search for factors that account for the reproduction and survival of mycobacteria, including vaccine strains, in host cells is the priority for studies on tuberculosis. A comparison of BCG-mycobacterial loads in granuloma cells obtained from bone marrow and spleens of mice with latent tuberculous infection and cells from mouse bone marrow and peritoneal macrophage cultures infected with the BCG vaccine in vitro has demonstrated that granuloma macrophages each normally contained a single BCG-Mycobacterium, while those acutely infected in vitro had increased mycobacterial loads and death rates. Mouse granuloma cells were observed to produce the IFNγ, IL-1α, GM-CSF, CD1d, CD25, CD31, СD35, and S100 proteins. None of these activation markers were found in mouse cell cultures infected in vitro or in intact macrophages. Lack of colocalization of lipoarabinomannan-labeled BCG-mycobacteria with the lysosomotropic LysoTracker dye in activated granuloma macrophages suggests that these macrophages were unable to destroy BCG-mycobacteria. However, activated mouse granuloma macrophages could control mycobacterial reproduction in cells both in vivo and in ex vivo culture. By contrast, a considerable increase in the number of BCG-mycobacteria was observed in mouse bone marrow and peritoneal macrophages after BCG infection in vitro, when no expression of the activation-related molecules was detected in these cells.

show abstract

Section: Resultsmentioning

confidence: 99%

Differences betweenMycobacterium-Host Cell Relationships in Latent Tuberculous Infection of MiceEx Vivoand Mycobacterial Infection of Mouse CellsIn Vitro

Ufimtseva

2016

Journal of Immunology Research

View full text Add to dashboard Cite

show abstract

“…As is known [2][3][4]9,19,34], TNFα-induced apoptosis of infected cells considerably reduces the bacterial load. However, overexpression of TNFα protein leads to the development of an uncontrollable inflammatory response in tissues and organs, which can result in the clinical signs of tuberculosis in man [2][3][4]34]. Therefore, proper regulation of the proinflammatory and costimulating activities of TNFα protein, as well as its proapoptotic effects depending on various factors acting on the cells in granulomatous inflammatory lesions is of major importance.…”

Section: Discussionmentioning

confidence: 99%

“…Apoptotic death of cells infected with mycobacteria is considered to be one of the main mechanisms by which an affected organism can withstand tuberculous infection [4,5,[7][8][9]24,25]. Apoptosis leads not only to disposal of digested apoptotic cells with mycobacteria and their elimination in phagosomes, but also to an efficient processing of mycobacterial antigens used by antigen-presenting cells for the maintenance and enhancement of the immune response to the pathogen [24].…”

Section: Discussionmentioning

confidence: 99%

“…by compromised cell membranes and nuclear envelopes, cytoplasmic swelling and cellular breakdown [22][23][24][25]. The apoptotic death of infected macrophages has been proposed to be one of the main mechanisms by which the organism controls tuberculous infection through depopulating pathogenic microorganisms and infected cells [4][5][7][8][9]25]. By contrast, the necrotic death of infected cells leads to the release of living bacteria into the extracellular environment and further spread of infection throughout animal and human organisms [5,[24][25][26][27][28].…”

mentioning

confidence: 99%

See 1 more Smart Citation

The Control of Apoptotic Death in the Cells of Granulomatous Inflammatory Lesions from Mice with Latent Tuberculous Infection in the Ex Vivo Model

Ufimtseva¹

2017

Immunome Res

View full text Add to dashboard Cite

Tuberculosis is a leading worldwide health problem. The latent, symptom-free stage of tuberculous infection is characterized by the formation of granulomas, specific aggregates of immune cells, predominantly macrophages, containing mycobacteria. The apoptotic death of macrophages containing mycobacteria is considered the main mechanism by which animals and human organisms oppose tuberculous infection and control its development. Previously, we have compared Mycobacterium-host cell relationships in individual granuloma cells from mice with latent tuberculous infection and cells from mouse bone marrow and peritoneal cultures infected with BCG vaccine in vitro and shown that increased death rates were revealed for macrophages heavily loaded with mycobacteria after acute BCG infection in vitro. While in ex vivo cultures granuloma macrophages with large numbers of BCG mycobacteria in them were still viable and had neither apoptotic nor necrotic morphology.Since different specific cellular responses to latent chronic and acute BCG infection in mouse cells were determined, the our aim was to analyze granulomas isolated from the lungs, spleens and bone marrow of Balb/c mice with latent BCG infection for the presence of inducers and markers of apoptotic cell death. In granuloma cells with increased levels of the inducer of apoptosis TNFα, proapoptotic proteins Вах and Ваd, death receptor Fas/ CD95 and scavenge receptor CD36, we did not observe P53 stabilization or caspase-3 activation in the cytoplasm or nuclei of macrophages and dendritic cells, irrespective of the presence or absence of acid-fast BCG mycobacteria in them. The survival receptor CD30 was detected on the cell membranes of only few granuloma macrophages. However, at later times of tuberculous infection in mice, virtually all macrophages and other granuloma cell types had considerable amounts of the antiapoptotic protein Bcl-2 in the cytoplasm and, probably, mitochondria, in contrast to macrophages from bone barrow cell cultures and peritoneal exudates infected with BCG mycobacteria in vitro. Preservation of mitochondrial ΔΨ m during staining of living granuloma macrophages containing large amounts of the Bcl-2 protein was indicative of its involvement in maintaining the integrity of mitochondrial elements and the protection of granuloma cells from death, because in similar experiments the control macrophages that did not have any Bcl-2 protein in them had considerably reduced ΔΨ m and exhibited morphological signs of apoptotic death. Taken together, our results suggest that the antiapoptotic protein Bcl-2 has been proposed to contribute to the viability of granulomas macrophages not only in ex vivo culture, but also in the animal organism when faced with mycobacterial, proinflammatory and proapoptotic factors operating in granulomatous inflammatory lesions at various times of latent tuberculous infection in mice. by compromised cell membranes and nuclear envelopes, cytoplasmic swelling and cellular breakdown [22][23][24][25]. The apoptotic death of...

show abstract

“…It is well established that adherence molecules (adhesins) play a fundamental role in the pathogen-host interaction (da Silva Neto et al, 2009;Espitia et al, 2012). Invasion of host cells by bacteria is a complex process involving both bacterial and host cell determinants (Bermudez & Goodman, 1996;Danelishvili et al, 2003).…”

Section: Introductionmentioning

confidence: 99%

Mycobacterium tuberculosis adhesins: potential biomarkers as anti-tuberculosis therapeutic and diagnostic targets

2014

View full text Add to dashboard Cite

Adhesion to host cells is a precursor to host colonization and evasion of the host immune response. Conversely, it triggers the induction of the immune response, a process vital to the host’s defence against infection. Adhesins are microbial cell surface molecules or structures that mediate the attachment of the microbe to host cells and thus the host–pathogen interaction. They also play a crucial role in bacterial aggregation and biofilm formation. In this review, we discuss the role of adhesins in the pathogenesis of the aetiological agent of tuberculosis, Mycobacterium tuberculosis. We also provide insight into the structure and characteristics of some of the characterized and putative M. tuberculosis adhesins. Finally, we examine the potential of adhesins as targets for the development of tuberculosis control strategies.

show abstract

Host–Pathogen Interactions in Tuberculosis

Cited by 8 publications

References 166 publications

Differences betweenMycobacterium-Host Cell Relationships in Latent Tuberculous Infection of MiceEx Vivoand Mycobacterial Infection of Mouse CellsIn Vitro

Differences betweenMycobacterium-Host Cell Relationships in Latent Tuberculous Infection of MiceEx Vivoand Mycobacterial Infection of Mouse CellsIn Vitro

The Control of Apoptotic Death in the Cells of Granulomatous Inflammatory Lesions from Mice with Latent Tuberculous Infection in the Ex Vivo Model

Mycobacterium tuberculosis adhesins: potential biomarkers as anti-tuberculosis therapeutic and diagnostic targets

Contact Info

Product

Resources

About