Neutrophil Response to <i>Pseudomonas aeruginosa</i> in Respiratory Infection

Ahmed, Kawsar; Dai, Tran Cong; Ichinose, Akitoyo; Masaki, Hironori; Nagatake, Tsuyoshi; Matsumoto, Keizō

doi:10.1111/j.1348-0421.1993.tb01672.x

Cited by 13 publications

(7 citation statements)

References 16 publications

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“…2). There is ample clinical evidence that luminal necrosis commonly occurs in inflammatory airway conditions [61][62][63][64]. Indeed, airway plugs are characteristically rich in disintegrating cells and cell debris [61][62][63][64][65][66][67][68].…”

Section: When Clearance Through Luminal Entry Goes Wrong: Luminal Necmentioning

confidence: 99%

Transepithelial Migration, Necrosis and Apoptosis as Silent and Pro- Inflammatory Fates of Airway Granulocytes

Erjefält

2005

CDTIA

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In inflammatory airway diseases, granulocytes such as eosinophils and neutrophils infiltrate the tissue where they are thought to exert pathogenic activities. To avoid a catastrophic accumulation of activated granulocytes, their recruitment must be balanced by efficient cell clearance mechanisms. In this regard, the focus has been on elimination through apoptosis and subsequent engulfment of apoptotic cells by phagocytes. However, novel data suggest that in the airways, powerful non-apoptotic mechanisms are also critically involved in cell clearance. One such mechanism is transepithelial migration into the airway lumen where the mucociliary escalator executes the final elimination. The physiological clearance of tissue granulocytes is normally silent, but can under certain situations shift to become a pro-inflammatory event. For example, apoptotic cells that escape phagocytosis, disintegrate in a pro-inflammatory process called secondary necrosis. In other situations, granulocytes are triggered to undergo an active and violent cytolytic death. This delicate balance in vivo, between silent and violent properties of granulocyte demise, complicates the design of pro-apoptotic pharmacological interventions. On the other hand, this insight may also open possibilities to new exciting treatment strategies. In this context, promoting transepithelial migration, prevention of secondary necrosis, and boosting the macrophage phagocytic system appear as exciting treatment avenues.

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Section: When Clearance Through Luminal Entry Goes Wrong: Luminal Necmentioning

confidence: 99%

Transepithelial Migration, Necrosis and Apoptosis as Silent and Pro- Inflammatory Fates of Airway Granulocytes

Erjefält

2005

CDTIA

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“…This is consistent with our result. By the same method used in the present study, structures suggestive of capsule were observed in Pseudomonas aeruginosa by the EM observation of sputum (2). It is reported that nontypable H. influenzae has undulant cell wall (12).…”

Section: Discussionmentioning

confidence: 69%

Neutrophil Response to Nontypable Haemophilus influenzae in Respiratory Infections

Ahmed

Ichinose

Dai

et al. 1993

Microbiology and Immunology

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Sputa from patients with respiratory infections by nontypable Haemophilus influenzae (H. influenzae) were investigated by electron microscopy. The cell wall of H. influenzae appeared wavy and nonwavy. In the cell wall the peptidoglycan layer was ill-defined. These patients had adequate IgG response in the serum against H. influenzae. However neither capsule nor fimbriae were found. Different stages of phagocytosis and destruction of the bacteria by polymorphonuclear neutrophils (PMN) were observed. PMNs were also found to phagocytose the debris. Evidences were found that the debris is formed mainly by the destruction of polymorphonuclear neutrophil. Extracellular lysosomes were also observed, which may have a role in destruction of both bacteria and host tissue. It was concluded that nontypable H. influenzae are nonfimbriated and noncapsulated during infection. Debris are the end product of PMN destruction, and phagocytosis of debris by PMNs has a role in the pathogenesis of chronic respiratory diseases.

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“…The absence of NE-mediated killing is likely attributed to production of the protease inhibitor ecotin by bacteria [64]. In addition, NET formation induced by P. aeruginosa depends strongly on flagella motility [65], which may further explain the absence of NETs in CF lungs in which the flagella of P. aeruginosa are down-regulated [66] and in which flagellin, which is the major component of flagella, may be cleaved by NE [67]. Since a decrease and/or absence of flagella motility is associated with formation of bacterial biofilms [68], a lack of motile flagella may lead to a lack of detectable NETs.…”

Section: Discussionmentioning

confidence: 99%

The origin of extracellular DNA in bacterial biofilm infectionsin vivo

Alhede

Qvortrup

Kragh

et al. 2019

Preprint

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35 Mobile +45 20 65 98 88 36 fax + 45 35 45 64 12 37 Tbjarnsholt@sund.ku.dk 38 www.sund.ku.dk 39 40 41 42 43 44 45 46 47 48 49 50 51 52 Abstract 53 Extracellular DNA (eDNA) plays an important role in both the aggregation of bacteria54 and in the interaction of the resulting biofilms with polymorphonuclear leukocytes 55 (PMNs) during an inflammatory response. Here, transmission electron and confocal 56 scanning laser microscopy were used to examine the interaction between biofilms of 57 Pseudomonas aeruginosa and PMNs in a murine implant model and in lung tissue from 3 58 chronically infected cystic fibrosis patients. PNA FISH, DNA staining, labeling of 59 PMN DNA with a thymidine analogue, and immunohistochemistry were applied to 60 localize bacteria, eDNA, PMN-derived eDNA, PMN-derived histone H3 (H3), 61 neutrophil elastase (NE), and citrullinated H3 (citH3). Host-derived eDNA was 62 observed surrounding bacterial aggregates but not within the biofilms. H3 localized to 63 the lining of biofilms while NE was found throughout biofilms. CitH3, a marker for 64 neutrophil extracellular traps (NETs) was detected only sporadically indicating that 65 most host-derived eDNA in vivo was not a result of NETosis. Together these 66 observations show that, in these in vivo biofilm infections with P. aeruginosa, the 67 majority of eDNA is found external to the biofilm and derives from the host. 68 69 70 71 Keywords: polymorphonuclear leukocytes/ neutrophil extracellular traps/ NETosis, 72 /Histone/ elastase 73 74 Author summary75 The role of extracellular DNA (eDNA) has been described in vitro to play a major role in 76 biofilm formation and antibiotic tolerance, but never for biofilm infections in vivo. 77 78 Two important characteristics of human chronic bacterial infections are aggregated 79 bacteria and white blood cells (WBC). Bacteria use eDNA to stabilize biofilms and WBC 80 use eDNA to trap bacteria. Given the importance of eDNA for both bacteria and WBC we 81 show here for the first time that bacterial biofilms do not co-localize with either bacterial 82 or WBC-derived eDNA during chronic infections. Our in vivo findings show eDNA is 83 located outside biofilms as opposed to incorporated within the biofilm as commonly 84 observed in vitro. 85 86 We believe that understanding the interplay between biofilms and WBC during chronic 87 infection is essential if we are to elucidate the mechanisms underlying persistent infection 88 and ascertain why WBC fail to eradicate bacteria; this will enable us to develop new 89 treatment strategies. 4 90 91 92 93

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Neutrophil Response to Pseudomonas aeruginosa in Respiratory Infection

Cited by 13 publications

References 16 publications

Transepithelial Migration, Necrosis and Apoptosis as Silent and Pro- Inflammatory Fates of Airway Granulocytes

Transepithelial Migration, Necrosis and Apoptosis as Silent and Pro- Inflammatory Fates of Airway Granulocytes

Neutrophil Response to Nontypable Haemophilus influenzae in Respiratory Infections

The origin of extracellular DNA in bacterial biofilm infectionsin vivo

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