• Tuberculosis and Respiratory Diseases
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• 제50권3호
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• pp.281-292
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• 2001

• Tuberculosis and Respiratory Diseases
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• 제66권2호
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• pp.83-92
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• 2009

• Tuberculosis and Respiratory Diseases
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• 제74권1호
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• pp.1-6
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• 2013

The concept on idiopathic pulmonary fibrosis (IPF) pathogenesis has progressed from chronic inflammation to aberrant wounding healing and even more to the current paradigms of a multifactorial and heterogeneous disease process. Despite the growth of clinical trials for IPF, most of the results, including N-acetylcysteine combination, warfarin, and bosentan, were disappointing. On the other hand, there have been a number of important developments; the foremost is the licensing of pirfenidone in Europe and Asia. In this article, we briefly review the recent knowledge of pathogenesis of IPF. We also summarize the recent clinical trials regarding the management of IPF.

• Tuberculosis and Respiratory Diseases
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• 제68권2호
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• pp.55-61
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• 2010

Background: The underlying pathogenesis of fat embolism-induced acute lung injury (ALI) has not been elucidated. In the present study, the pathogenesis of fat embolism-induced ALI was probed in association with neutrophilic oxidative stress in oleic acid (OA)-induced ALI of S-D rats. Methods: OA was injected intravenously to provoke ALI in experimental rats. Five hours later, indices of ALI were measured to confirm the role of the neutrophilic respiratory burst. The effect of an inhibition of phospholipase A2 (PLA2) was also evaluated. Results: The accumulation of neutrophils in the lung due to OA caused increased neutrophilic oxidative stress in lung, which was ameliorated by mepacrine. What were the results from inhibition of PLA2. Conclusion: Excess neutrophilic oxidative stress contributes to OA-induced ALI, which is lessened by the inhibition of PLA2.

• Tuberculosis and Respiratory Diseases
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• 제85권4호
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• pp.320-331
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• 2022

Coronavirus disease 2019 (COVID-19) has become a major health burden worldwide, with over 450 million confirmed cases and 6 million deaths. Although the acute phase of COVID-19 management has been established, there is still a long way to go to evaluate the long-term clinical course or manage complications due to the relatively short outbreak of the virus. Pulmonary fibrosis is one of the most common respiratory complications associated with COVID-19. Scarring throughout the lungs after viral or bacterial pulmonary infection have been commonly observed, but the prevalence of post-COVID-19 pulmonary fibrosis is rapidly increasing. However, there is limited information available about post-COVID-19 pulmonary fibrosis, and there is also a lack of consensus on what condition should be defined as post-COVID-19 pulmonary fibrosis. During a relatively short follow-up period of approximately 1 year, lesions considered related to pulmonary fibrosis often showed gradual improvement; therefore, it is questionable at what time point fibrosis should be evaluated. In this review, we investigated the epidemiology, risk factors, pathogenesis, and management of post-COVID-19 pulmonary fibrosis.

• Tuberculosis and Respiratory Diseases
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• 제67권4호
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• pp.275-280
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• 2009

Interstitial lung disease (ILD) is a group of diseases characterized by pulmonary interstitial inflammation. Finally the inflammation results in pulmonary fibrosis and impairment of oxygen transportation. The causes of idiopathic interstitial pneumonia (IIP) are unknown. Diagnosis of IIP is not easy, especially distinguising between nonspecific interstitial pneumonia and usual interstitial pneumonia (UIP). First line treatments of IIP include corticosteroids and immune modulators, which have limited effect. Currently, several drugs are being researched to prevent and treat fibrosis. Newer drugs that may useful to treat pulmonary fibrosis include endothelin receptor antagonist, recombinant soluble TNF receptor antagonist, and cotrimoxazole. The causes of IIP are largely unknown, treatment is not specific, and prognosis is poor. Recent studies are underway to investigate the pathogenesis and treatment of IIP and pulmonary fibrosis. As the pathogenesis of IIP is elucidated, better treatments will emerge.

• Tuberculosis and Respiratory Diseases
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• 제69권5호
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• pp.323-330
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• 2010

A key mechanism in the pathogenesis of chronic obstructive pulmonary disease is thought to be an abnormal inflammatory response in the lungs to the inhalation of toxic particles and gases, derived from tobacco smoke, air pollution, and/or occupational exposures. This review highlights the potential participation of several alternative pathogenetic processes, particularly involving the potential participation of biological and pathobiological processes related to aging, including oxidative stress and enhanced expression of markers of senescence/aging in emphysematous lungs, and the potential for enhanced tissue destruction involving alveolar cell apoptosis.

• 대한수의학회지
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• 제39권2호
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• pp.318-326
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• 1999

Respiratory pathogenic effects of several porcine reproductive and respiratory syndrome virus(PRRSV) isolates were examined in swine tracheal ring(STR) cultures by examining their effect on ciliary activity. One high and one low pathogenic PRRSV isolates were then selected and their pathogenicity investigated in 3-week-old conventional PRRSV-seronegative pigs. Ten pigs each were inoculated intranasally with the high or low pathogenic PRRSV isolate and 6 pigs were sham inoculated as negative controls. Two pigs each from the inoculated group and one pig each from negative control group were killed on 4, 7, 14, 21 and 28 days postinoculation(pI). At necropsy, degrees of gross lung lesion was determined. Turbinate, tonsil, trachea and lung samples were collected for virus isolation or histopathology. Gross lung lesions were observed mainly on 14 days PI with high and low pathogenic isolates inducing moderate diffuse and mild gross lung lesions, respectively. Inoculation of either the high or low pathogenic virus resulted in loss of cilia in ciliated epithelium of turbinates and trachea between 7 and 28 days PI. High pathogenic virus caused increased number of Goblet cells in the tracheal epithelial layer between 4 and 21 days PI whereas the low pathogenic virus did it between 14 and 28 days PI and with a lesser degree. Although both viruses produced interstitial pneumonia, the lesion was less severe with the low pathogenic virus. The isolation of high pathogenic virus from tissues and sera was earlier and more consistent than that of the low pathogenic virus. The agreement between in vitro and in vivo tests indicates that STR cultures may be used as a routine method to determine the respiratory pathogenicity of PRRSV isolates.

• Tuberculosis and Respiratory Diseases
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• 제79권2호
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• pp.53-57
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• 2016

Severe sepsis or septic shock is characterized by an excessive inflammatory response to infectious pathogens. Acute respiratory distress syndrome (ARDS) is a devastating complication of severe sepsis, from which patients have high mortality. Advances in treatment modalities including lung protective ventilation, prone positioning, use of neuromuscular blockade, and extracorporeal membrane oxygenation, have improved the outcome over recent decades, nevertheless, the mortality rate still remains high. Timely treatment of underlying sepsis and early identification of patients at risk of ARDS can help to decrease its development. In addition, further studies are needed regarding pathogenesis and novel therapies in order to show promising future treatments of sepsis-induced ARDS.

• BMB Reports
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• 제44권4호
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• pp.232-237
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• 2011

Human respiratory syncytial virus (HRSV) is a major cause of upper and lower respiratory tract illness in infants and young children worldwide. Despite its importance as a respiratory pathogen, there is currently no licensed vaccine for prophylaxis of HRSV infection. There are several hurdles complicating the development of a RSV vaccine: 1) incomplete immunity to natural RSV infection leading to frequent re-infection, 2) immature immune system and maternal antibodies of newborn infants who are the primary subject population, and 3) imbalanced Th2-biased immune responses to certain vaccine candidates leading to exacerbated pulmonary disease. After the failure of an initial trial featuring formalin-inactivated virus as a RSV vaccine, more careful and deliberate efforts have been made towards the development of safe and effective RSV vaccines without vaccine-enhanced disease. A wide array of RSV vaccine strategies is being developed, including live-attenuated viruses, protein subunit-based, and vector-based candidates. Though licensed vaccines remain to be developed, our great efforts will lead us to reach the goal of attaining safe and effective RSV vaccines in the near future.