Fibronectin Facilitates<i>Mycobacterium tuberculosis</i>Attachment to Murine Alveolar Macrophages

Pasula, Rajamouli; Wisniowski, Paul; Martin, William J.

doi:10.1128/iai.70.3.1287-1292.2002

Cited by 31 publications

(25 citation statements)

References 54 publications

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“…As shown in Figure 10B, the LGTIPG peptide at a concentration of 10 μM increased migration activity, while the YIGSR peptide and intact laminin had only a weak or negligible effect on activity. Similarly, as demonstrated in previous studies (24,25,35), the RGDS peptide at concentrations of 0.1 μM and 1 μM enhanced migration activity, whereas the RGES peptide and intact fibronectin had a negligible effect on activity ( Figure 10B). To study the involvement of these peptides in macrophage migration, we performed an inhibition study by incubating…”

Section: Figuresupporting

confidence: 89%

Targeted deletion or pharmacological inhibition of MMP-2 prevents cardiac rupture after myocardial infarction in mice

Matsumura¹,

Iwanaga²,

Mochizuki³

et al. 2005

J. Clin. Invest.

139

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MMPs are implicated in LV remodeling after acute myocardial infarction (MI).To analyze the role of MMP-2, we generated MI by ligating the left coronary artery of MMP-2-KO and WT mice, the latter of which were administered orally an MMP-2-selective inhibitor or vehicle (TISAM). The survival rate was significantly higher in MMP-2-KO and TISAM-treated mice than in control WT mice. The main cause of mortality in control WT mice was cardiac rupture, which was not observed in MMP-2-KO or TISAM-treated mice. Control WT mice, but not MMP-2-KO or TISAM-treated mice, showed activation of the zymogen of MMP-2, strong gelatinolytic activity, and degradation of ECM components, including laminin and fibronectin, in the infarcted myocardium. Although infarcted cardiomyocytes in control WT mice were rapidly removed by macrophages, the removal was suppressed in MMP-2-KO and TISAM-treated mice. Macrophage migration was induced by the infarcted myocardial tissue from control WT mice and was inhibited by treatment of macrophages with laminin or fibronectin peptides prior to migration assay. These data suggest that inhibition of MMP-2 activity improves the survival rate after acute MI by preventing cardiac rupture and delays post-MI remodeling through a reduction in macrophage infiltration.

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Section: Figuresupporting

confidence: 89%

Targeted deletion or pharmacological inhibition of MMP-2 prevents cardiac rupture after myocardial infarction in mice

Matsumura¹,

Iwanaga²,

Mochizuki³

et al. 2005

J. Clin. Invest.

139

View full text Add to dashboard Cite

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“…Their ability to subsist within macrophages is attributed to the striking ability of the mycobacteria to arrest phagosome maturation at an early stage, thereby avoiding the delivery of microbicidal effectors found in mature phagolysosomes. M. tuberculosis- (91,99), and scavenger receptors (138). However, members of the complement receptor family, i.e., CR1, CR3, and CR4, have most commonly been observed to facilitate mycobacterial uptake (45,106,107).…”

Section: Mycobacterium Tuberculosismentioning

confidence: 99%

Regulation of Vacuolar pH and Its Modulation by Some Microbial Species

Huynh

Grinstein

2007

Microbiol Mol Biol Rev

133

134

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SUMMARYTo survive within the host, pathogens such asMycobacterium tuberculosisandHelicobacter pylorineed to evade the immune response and find a protected niche where they are not exposed to microbicidal effectors. The pH of the microenvironment surrounding the pathogen plays a critical role in dictating the organism's fate. Specifically, the acidic pH of the endocytic organelles and phagosomes not only can affect bacterial growth directly but also promotes a variety of host microbicidal responses. The development of mechanisms to avoid or resist the acidic environment generated by host cells is therefore crucial to the survival of many pathogens. Here we review the processes that underlie the generation of organellar acidification and discuss strategies employed by pathogens to circumvent it, usingM. tuberculosisandH. pylorias examples.

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“…Many pathogenic bacteria have evolved surface molecules or receptors capable of binding host proteins that enhance adherence, colonization, and invasion of host epithelial surfaces (15,26,33). For instance, binding to fibronectin by pathogenic bacteria can enhance initial colonization of the epithelial cells on mucosal surfaces (12,22,25,30) and trigger cellular invasion (33). In any event, these observations have radically altered the way we think about the surface architecture of M. hyopneumoniae.…”

Section: Vol 72 2004mentioning

confidence: 99%

Proteolytic Processing of the Mycoplasma hyopneumoniae Cilium Adhesin

et al. 2004

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Mycoplasma hyopneumoniae is an economically significant swine pathogen that colonizes the respiratory ciliated epithelial cells. Cilium adherence is mediated by P97, a surface protein containing a repeating element (R1) that is responsible for binding. Here, we show that the cilium adhesin is proteolytically processed on the surface. Proteomic analysis of strain J proteins identified cleavage products of 22, 28, 66, and 94 kDa. N-terminal sequencing showed that the 66-and 94-kDa proteins possessed identical N termini and that the 66-kDa variant was generated by cleavage of the 28-kDa product from the C terminus. The 22-kDa product represented the N-terminal 195 amino acids of the cilium adhesin preprotein, confirming that the hydrophobic leader signal sequence is not cleaved during translocation across the membrane. Comparative studies of M. hyopneumoniae strain 232 showed that the major cleavage products of the cilium adhesin are similar, although P22 and P28 appear to be processed further in strain 232. Immunoblotting studies using antisera raised against peptide sequences within P22 and P66/P94 indicate that processing is complex, with cleavage occurring at different frequencies within multiple sites, and is strain specific. Immunogold electron microscopy showed that fragments containing the cilium-binding site remained associated with the cell surface whereas cleavage products not containing the R1 element were located elsewhere. Not all secreted proteins undergo multiple cleavage, however, as evidenced by the analysis of the P102 gene product. The ability of M. hyopneumoniae to selectively cleave its secreted proteins provides this pathogen with a remarkable capacity to alter its surface architecture.Mycoplasma hyopneumoniae, the etiological agent of enzootic pneumonia, significantly impacts swine production (28). During colonization, M. hyopneumoniae forms an intricate association with the ciliated epithelial lining of the porcine respiratory tract, leading to chronic respiratory disease. Colonization disrupts the normal function of the mucociliary escalator through ciliostasis, loss of cilia, epithelial cell death, and acute inflammation. This results in a purulent exudate (composed primarily of neutrophils and mononuclear cells) in the airways (17). Disease resolution occurs only after a prolonged period (if at all). M. hyopneumoniae colonization also predisposes the host to more-severe infections from secondary pathogens (2). For example, it is now clear that colonization by M. hyopneumoniae leads to more-severe and longer-lasting disease with the porcine respiratory and reproductive syndrome virus (34). Thus, the impact of M. hyopneumoniae on swine production has not been fully realized.It is known that the initial event in colonization by M. hyopneumoniae is binding to swine respiratory cilia (19,32). In the absence of binding activity, colonization does not occur (38). Identification of the molecules involved in cilium binding occurred only after the discovery of adherence-blocking monoclonal antibod...

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Fibronectin FacilitatesMycobacterium tuberculosisAttachment to Murine Alveolar Macrophages

Cited by 31 publications

References 54 publications

Targeted deletion or pharmacological inhibition of MMP-2 prevents cardiac rupture after myocardial infarction in mice

Targeted deletion or pharmacological inhibition of MMP-2 prevents cardiac rupture after myocardial infarction in mice

Regulation of Vacuolar pH and Its Modulation by Some Microbial Species

Proteolytic Processing of the Mycoplasma hyopneumoniae Cilium Adhesin

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