Clinicopathological Findings of Four Cases of Pure Influenza Virus A Pneumonia

Fujita, Jiro; Ohtsuki, Yuji; Higa, Hajime; Azuma, Masato; Yoshinouchi, Takeo; Haranaga, Shusaku; Higa, Futoshi; Tateyama, Masao

doi:10.2169/internalmedicine.53.1174

Cited by 17 publications

(15 citation statements)

References 26 publications

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“…Patients infected with IAV commonly have alveolar hemorrhage, and this is a complication of influenza pneumonia, particularly with the H1N1 strain [13,[45][46][47][48][49][50]. Importantly, retrospective studies have shown an association between alveolar hemorrhages and increased mortality [51,52].…”

Section: Discussionmentioning

confidence: 99%

Tissue factor deficiency increases alveolar hemorrhage and death in influenza A virus‐infected mice

Antoniak

Tatsumi

Hisada

et al. 2016

Journal of Thrombosis and Haemostasis

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Background Influenza A virus (IAV) infection is a common respiratory tract infection that causes considerable morbidity and mortality worldwide. Objective To investigate the effect of a genetic deficiency of tissue factor (TF) in a mouse model of influenza A infection. Methods Wild-type mice, low tissue factor (LTF) mice and mice with the TF gene deleted in different cell types were infected with a mouse-adapted A/Puerto Rico/8/34 H1N1 strain of IAV. TF expression was measured in the lungs, and bronchoalveolar lavage fluid (BALF) was collected to measure extracellular vesicle TF, activation of coagulation, alveolar hemorrhage and inflammation. Results IAV infection of wild-type mice increased lung TF expression, activation of coagulation and inflammation in the BALF, but also led to alveolar hemorrhage. LTF mice and mice with a selective deficiency of TF in lung epithelial cells had low basal levels of TF and failed to increase TF expression after infection; these two strains of mice had more alveolar hemorrhage and death compared with controls. In contrast, deletion of TF in either myeloid cells or endothelial cells and hematopoietic cells did not increase alveolar hemorrhage or death after IAV infection. These results indicate that TF expression in the lung, particularly in epithelial cells, is required to maintain alveolar hemostasis after IAV infection. Conclusion Our study indicates that TF-dependent activation of coagulation is required to limit alveolar hemorrhage and death after influenza A infection.

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Section: Discussionmentioning

confidence: 99%

Tissue factor deficiency increases alveolar hemorrhage and death in influenza A virus‐infected mice

Antoniak

Tatsumi

Hisada

et al. 2016

Journal of Thrombosis and Haemostasis

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“…Viral infection due to influenza, respiratory syncytial virus, and some coronavirus can lead to diffuse alveolar damage (DAD) and hemorrhage [24][25][26][27][28][29]. DAD begins with an acute or exudative phase, wherein fibrin is deposited within the airways preventing air exchange.…”

Section: Mechanisms Of Carv-mediated Allograft Dysfunctionmentioning

confidence: 99%

“…DAD begins with an acute or exudative phase, wherein fibrin is deposited within the airways preventing air exchange. Epithelial cell damage may then follow, leading to deposition of a hyaline membrane [29]. If these depositions are not cleared, an organizing phase of DAD develops with proliferation of smooth muscle cells and promotion of immature alveolar type II cells [29], followed by deposition of collagen and ultimately fibrosis.…”

Section: Mechanisms Of Carv-mediated Allograft Dysfunctionmentioning

confidence: 99%

“…Epithelial cell damage may then follow, leading to deposition of a hyaline membrane [29]. If these depositions are not cleared, an organizing phase of DAD develops with proliferation of smooth muscle cells and promotion of immature alveolar type II cells [29], followed by deposition of collagen and ultimately fibrosis. It is not yet clear which pathways are key determinants of the progression from DAD to fibrosis.…”

Section: Mechanisms Of Carv-mediated Allograft Dysfunctionmentioning

confidence: 99%

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Infectious Triggers of Chronic Lung Allograft Dysfunction

Gregson

2016

Curr Infect Dis Rep

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Survival after lung transplantation is limited in large part due to the high incidence of chronic rejection, known as chronic lung allograft dysfunction (CLAD). Pulmonary infections are a frequent complication in lung transplant recipients, due both to immunosuppressive medications and constant exposure of the lung allograft to the external environment via the airways. Infection is a recognized risk factor for the development of CLAD, and both acute infection and chronic lung allograft colonization with microorganisms increase the risk for CLAD. Acute infection by community acquired respiratory viruses, and the bacteria Pseudomonas aeruginosa and Staphylococcus aureus are increasingly recognized as important risk factors for CLAD. Colonization by the fungus Aspergillus may also augment the risk of CLAD. Fostering this transition from healthy lung to CLAD in each of these infectious episodes is the persistence of an inflammatory lung allograft environment.

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“…Furthermore, HMs in DAD have usually been found in clinical acute respiratory distress syndrome, [3][4][5] acute exacerbation of usual interstitial pneumonia (UIP), 6 or rheumatoid arthritis-associated interstitial pneumonia, viral 7 and/ or bacterial pneumonia, and in infected lungs in malignant diseases, including leukemic cell infiltration in the lung and other kinds of pulmonary or extrapulmonary cancers. 1 Recently, DAD was categorized into 2 groups: primary (infection) and secondary (chemotherapy or druginduced).…”

Section: Introductionmentioning

confidence: 99%

Early Stages of Hyaline Membrane Formation Detected in Alveolar Mouths in Diffuse Alveolar-Damage-Associated Diseases

et al. 2015

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To study the early stages of hyaline membrane (HM) formation, diffuse alveolar damage (DAD) was thoroughly investigated using immunohistochemical methods in 15 autopsy cases, which consisted of various types of interstitial pneumonias and pulmonary diseases derived from nonmalignant or malignant diseases. Alveolar mouths (AMs) that were presumed to be normal were ultrastructurally examined in detail, by using pulmonary tissues in the pneumothorax. It is interesting to note that during the initial stages of HM formation in AMs, fragmented eosinophilic masses were closely attached to AMs as irregular fragments or by a cap-like structure. The ultrastructure revealed some distance between the capillary spaces and surface epithelium of the AMs, indicating that the epithelial cells at the AMs might be often easily damaged even by minor stimuli; they can be considered as "locus minoris resistentiae." HMs were found to be formed initially at the site of AMs derived from fragmented eosinophilic masses in not only pulmonary but also extrapulmonary diseases, including both nonmalignant and malignant diseases. These irregular eosinophilic masses, representing the early shape of HMs, were immunohistochemically positive for the epithelial membrane antigens, namely, surfactant protein A and factor VIII antigen, and occasionally for KL-6 and cytokeratins. These results suggested that fragmented irregular masses represent the initial phase of HM formation. Five of 15 cases were focally negative for KL-6 at the initial irregular mass of HMs. Because KL-6 is one of the fundamental components of pulmonary surface elements, it needs to be studied further by detailed clinicopathological examination.

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Clinicopathological Findings of Four Cases of Pure Influenza Virus A Pneumonia

Cited by 17 publications

References 26 publications

Tissue factor deficiency increases alveolar hemorrhage and death in influenza A virus‐infected mice

Tissue factor deficiency increases alveolar hemorrhage and death in influenza A virus‐infected mice

Infectious Triggers of Chronic Lung Allograft Dysfunction

Early Stages of Hyaline Membrane Formation Detected in Alveolar Mouths in Diffuse Alveolar-Damage-Associated Diseases

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