In this study, we examined the biological action of IL-17 on human non-small cell lung cancer (NSCLC). Although IL-17 had no direct effect on the in vitro growth rate of NSCLC, IL-17 selectively augmented the secretion of an array of angiogenic CXC chemokines, including CXCL1, CXCL5, CXCL6, and CXCL8 but not angiostatic chemokines, by three different NSCLC lines. Endothelial cell chemotactic activity (as a measure of net angiogenic potential) was increased in response to conditioned medium from NSCLC stimulated with IL-17 compared with those from unstimulated NSCLC. Enhanced chemotactic activity was suppressed by neutralizing mAb(s) to CXCL1, CXCL5, and CXCL8 or to CXCR-2 but not to vascular endothelial growth factor-A. Transfection with IL-17 into NSCLC had no effect on the in vitro growth, whereas IL-17 transfectants grew more rapidly compared with controls when transplanted in SCID mice. This IL-17-elicited enhancement of NSCLC growth was associated with increased tumor vascularity. Moreover, treatment with anti-mouse CXCR-2-neutralizing Ab significantly attenuated the growth of both neomycin phosphotransferase gene-transfected and IL-17-transfected NSCLC tumors in SCID mice. A potential role for IL-17 in modulation of the human NSCLC phenotype was supported by the findings that, in primary NSCLC tissues, IL-17 expression was frequently detected in accumulating and infiltrating inflammatory cells and that high levels of IL-17 expression were associated with increased tumor vascularity. These results demonstrate that IL-17 increases the net angiogenic activity and in vivo growth of NSCLC via promoting CXCR-2-dependent angiogenesis and suggest that targeting CXCR-2 signaling may be a novel promising strategy to treat patients with NSCLC.

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The minimum ADC of malignant astrocytomas can provide additional information about their clinical malignancy related to posttreatment prognosis.

On May 22, 2020, this report was posted as an MMWR Early Release on the MMWR website (https://www.cdc.gov/mmwr). On March 28, 2020, two residents of a long-term care skilled nursing facility (SNF) at the Veterans Affairs Greater Los Angeles Healthcare System (VAGLAHS) had positive test results for SARS-CoV-2, the cause of coronavirus disease 2019 (COVID-19), by reverse transcription-polymerase chain reaction (RT-PCR) testing of nasopharyngeal specimens collected on March 26 and March 27. During March 29-April 23, all SNF residents, regardless of symptoms, underwent serial (approximately weekly) nasopharyngeal SARS-CoV-2 RT-PCR testing, and positive results were communicated to the county health department. All SNF clinical and nonclinical staff members were also screened for SARS-CoV-2 by RT-PCR during March 29-April 10. Nineteen of 99 (19%) residents and eight of 136 (6%) staff members had positive test results for SARS-CoV-2 during March 28-April 10; no further resident cases were identified on subsequent testing on April 13, April 22, and April 23. Fourteen of the 19 residents with COVID-19 were asymptomatic at the time of testing. Among these residents, eight developed symptoms 1-5 days after specimen collection and were later classified as presymptomatic; one of these patients died. This report describes an outbreak of COVID-19 in an SNF, with case identification accomplished by implementing several rounds of RT-PCR testing, permitting rapid isolation of both symptomatic and asymptomatic residents with COVID-19. The outbreak was successfully contained following implementation of this strategy. VAGLAHS includes 150 long-term care beds in three SNF patient care areas, or wards; SNF wards A and B are in building 1, and ward C is in building 2. Buildings 1 and 2 do not share common areas, but residents might have indirect contact with outside persons while receiving medical services such as dialysis. These wards admit residents who require intravenous antibiotics, complex wound care, other rehabilitation needs, routine dialysis, chemotherapy, or radiation therapy; underlying conditions, including chronic obstructive pulmonary disease, hypertension, cardiovascular disease, and chronic kidney disease, are common. At the time of the outbreak, 99 (66%) beds were occupied; >95% of residents were men aged 50-100 years. All data were abstracted from the VAGLAHS

Excessive production of airway mucus is a cardinal feature of bronchial asthma and chronic obstructive pulmonary disease (COPD) and contributes to morbidity and mortality in these diseases. IL-13, a Th2-type cytokine, is a central mediator in the pathogenesis of bronchial asthma, including mucus overproduction. Using a genome-wide search for genes induced in airway epithelial cells in response to IL-13, we identified pendrin encoded by the SLC26A4 (PDS) gene as a molecule responsible for airway mucus production. In both asthma and COPD mouse models, pendrin was up-regulated at the apical side of airway epithelial cells in association with mucus overproduction. Pendrin induced expression of MUC5AC, a major product of mucus in asthma and COPD, in airway epithelial cells. Finally, the enforced expression of pendrin in airway epithelial cells in vivo, using a Sendai virus vector, rapidly induced mucus overproduction in the lumens of the lungs together with neutrophilic infiltration in mice. These findings collectively suggest that pendrin can induce mucus production in airway epithelial cells and may be a therapeutic target candidate for bronchial asthma and COPD.