Pseudomonas aeruginosa Induces Interferon-β Production to Promote Intracellular Survival

Yang, Ling; Zhang, Yu-Wei; Liu, Yang; Xie, Ying-Zhou; Weng, Dagen; Ge, Baoxue; Liu, Haipeng; Xu, Jin

doi:10.1128/spectrum.01550-22

Cited by 3 publications

(2 citation statements)

References 47 publications

(55 reference statements)

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“…Interleukin-1β is a pro-inflammatory cytokine activated by the Nod-like receptor, pyrin domain containing three and Nod-like receptor, containing four inflammatory complex. Yang et al discovered that the innate immunity factor, interferon-beta, promotes the cytoplasmic survival of Pseudomonas aeruginosa in macrophages and that its production is inhibited [ 21 ]. These findings establish a connection between innate immunity and Pseudomonas aeruginosa .…”

Section: Discussionmentioning

confidence: 99%

Analysis of clinical characteristics, prognosis and influencing factors in patients with bronchiectasis-chronic obstructive pulmonary disease overlap syndrome: A prospective study for more than five years

Dai,

Zhong,

Cui

et al. 2024

J Glob Health

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Section: Discussionmentioning

confidence: 99%

Analysis of clinical characteristics, prognosis and influencing factors in patients with bronchiectasis-chronic obstructive pulmonary disease overlap syndrome: A prospective study for more than five years

Dai,

Zhong,

Cui

et al. 2024

J Glob Health

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“…It is well established that PA is an intracellular pathogen that can survive and replicate inside of epithelial cells [38,39]. These processes are mediated in part by virulence factors [7,[40][41][42]. To determine whether EVs released by PA-infected host cells conferred a protective or deleterious effect on PA invasion of hTCEpi cells or HBECs, we next performed a gentamicin invasion assay.…”

Section: Innate Immune Responses In Corneal and Bronchial Epithelial ...mentioning

confidence: 99%

Extracellular vesicles released by host epithelial cells during Pseudomonas aeruginosa infection function as homing beacons for neutrophils

Ayilam Ramachandran,

Lemoff,

Robertson

2024

Cell Commun Signal

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Background Pseudomonas aeruginosa (PA) is an opportunistic pathogen that can cause sight threatening infections in the eye and fatal infections in the cystic fibrosis airway. Extracellular vesicles (EVs) are released by host cells during infection and by the bacteria themselves; however, there are no studies on the composition and functional role of host-derived EVs during PA infection of the eye or lung. Here we investigated the composition and capacity of EVs released by PA infected epithelial cells to modulate innate immune responses in host cells. Methods Human telomerase immortalized corneal epithelial cells (hTCEpi) cells and human telomerase immortalized bronchial epithelial cells (HBECs) were treated with a standard invasive test strain of Pseudomonas aeruginosa, PAO1, for 6 h. Host derived EVs were isolated by qEV size exclusion chromatography. EV proteomic profiles during infection were compared using mass spectrometry and functional studies were carried out using hTCEpi cells, HBECs, differentiated neutrophil-like HL-60 cells, and primary human neutrophils isolated from peripheral blood. Results EVs released from PA infected corneal epithelial cells increased pro-inflammatory cytokine production in naïve corneal epithelial cells and induced neutrophil chemotaxis independent of cytokine production. The EVs released from PA infected bronchial epithelial cells were also chemotactic although they failed to induce cytokine secretion from naïve HBECs. At the proteomic level, EVs derived from PA infected corneal epithelial cells exhibited lower complexity compared to bronchial epithelial cells, with the latter having reduced protein expression compared to the non-infected control. Conclusions This is the first study to comprehensively profile EVs released by corneal and bronchial epithelial cells during Pseudomonas infection. Together, these findings show that EVs released by PA infected corneal and bronchial epithelial cells function as potent mediators of neutrophil migration, contributing to the exuberant neutrophil response that occurs during infection in these tissues.

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Context‐specific anti‐inflammatory roles of type III interferon signaling in the lung in nonviral injuries

Feng,

Kim,

Wang

et al. 2024

Physiological Reports

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Type III interferons (λ1, λ2, and λ3) are potent antiviral cytokines in the lung. However, their roles in nonviral lung injuries are less well understood. This study investigates the activation of type III interferon signaling in three distinct models of lung injuries caused by diverse stimuli: the bacterial pathogen Pseudomonas aeruginosa, bacterial endotoxin LPS, and the chemotherapeutic agent bleomycin. Our data show that, despite inducing a potent inflammatory response, Pseudomonas and LPS did not increase IFNλ secretion. In contrast, bleomycin instillation increased secretion of IFNλ in the airways at both early and late time points. Consistent with limited secretion, type III interferon signaling had a minimal role in the host response to both Pseudomonas and LPS, as measured by pathogen burden, inflammatory response, and lung injury. Conversely, a deficiency in type III interferon signaling led to increased inflammatory signaling and elevated acute lung injury in the bleomycin model on day 3. This elevated early injury resulted in impaired recovery in IFNLR1 knockout mice, as evidenced by their recovery from bleomycin‐induced weight loss. Taken together, these data suggest a context‐specific activation of type III interferon signaling, where it plays an anti‐inflammatory role in the lung.

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Pseudomonas aeruginosa Induces Interferon-β Production to Promote Intracellular Survival

Cited by 3 publications

References 47 publications

Analysis of clinical characteristics, prognosis and influencing factors in patients with bronchiectasis-chronic obstructive pulmonary disease overlap syndrome: A prospective study for more than five years

Analysis of clinical characteristics, prognosis and influencing factors in patients with bronchiectasis-chronic obstructive pulmonary disease overlap syndrome: A prospective study for more than five years

Extracellular vesicles released by host epithelial cells during Pseudomonas aeruginosa infection function as homing beacons for neutrophils

Context‐specific anti‐inflammatory roles of type III interferon signaling in the lung in nonviral injuries

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