In this task, you're given a paragraph from the research paper and your task is to generate a suitable title for the research paper based on the given paper. Under 100 words is a good title length.

Acute cough is a major symptom of viral respiratory tract infection and causes excessive morbidity in human populations across the world. A wide variety of viruses play a role in the development of cough after acute infection and all of these manifest a similar clinical picture across different age groups. Despite the large disease burden surprisingly little is known about the mechanism of acute cough following viral infection. Both in vitro and in vivo experiments show that increased production of neuropeptides and leukotrienes mediate cough after viral infection, along with altered expression of neural receptors. Increased airway mucus production is also likely to play a significant role. This work is reviewed in this article. Following the recent development of a mouse model for rhinovirus infection and the establishment of experimental models of rhinovirus challenge in human subjects with both asthma and COPD the field is expanding to translate in vitro research into clinical studies and hopefully eventually into clinical practice. Developing a clearer understanding of the mechanisms underlying virus induced cough may lead to more specific and effective therapies.
Cough and viruses in airways disease: Mechanisms

Ca 2+ is one of the most universal and versatile signaling molecules and is involved in almost every aspect of cellular processes. Viruses are adept at utilizing the universal Ca 2+ signal to create a tailored cellular environment that meets their own demands. This review summarizes most of the known mechanisms by which viruses perturb Ca 2+ homeostasis and utilize Ca 2+ and cellular Ca 2+ -binding proteins to their benefit in their replication cycles. Ca 2+ plays important roles in virion structure formation, virus entry, viral gene expression, posttranslational processing of viral proteins and virion maturation and release. As part of the review, we introduce an algorithm to identify linear "EF-hand" Ca 2+ -binding motifs which resulted in the prediction of a total of 93 previously unrecognized Ca 2+ -binding motifs in virus proteins. Many of these proteins are nonstructural proteins, a class of proteins among which Ca 2+ interactions had not been formerly appreciated. The presence of linear Ca 2+ -binding motifs in viral proteins enlarges the spectrum of Ca 2+ -virus interplay and expands the total scenario of viral calciomics. (J.J. Yang). for structural integrity or functionality; and (3) critical virus-host interactions depend on cellular Ca 2+ -regulated proteins or pathways. This review, which aims to stimulate future studies on the roles of Ca 2+ in virus infection, is focused on such interplay by highlighting recent discoveries in the biological roles of Ca 2+ in virus infection. 0143-4160/$ -see front matter
Viral calciomics: Interplays between Ca 2+ and virus

Background: Mesenchymal stem cells (MSCs) might act as fine-tuners of inflammation during acute lung injury. We assessed the effects of adoptive transfer of MSCs in acid aspiration acute lung injury and explored the role of long pentraxin PTX3. Methods: We conducted a prospective experimental interventional study on wildtype (WT) and PTX3-deficient (PTX3 −/− ) mice. Acute lung injury was induced in WT and PTX3 −/− mice by instillation of hydrochloric acid into the right bronchus. One hour later, animals received intraperitoneal sterile phosphate-buffered saline (PBS), WT-MSCs (1 × 10 6 ) or PTX3 −/− -MSCs (1 × 10 6 ). Twenty-four hours after injury, we measured the effects of treatments on arterial blood gases, wet/dry lung weight (W/ D), CT scan analysis of lung collapse, neutrophils, TNFα and CXCL1 in bronchoalveolar lavage, and plasma PTX3. D-dimer was assayed in 1 week and OHproline in 2 weeks to track the fibrotic evolution. Results: In 24 h, in comparison to PBS, WT-MSCs improved oxygenation and reduced W/D and alveolar collapse. These effects were associated with decreased concentrations of alveolar neutrophils and cytokines. WT-MSCs increased D-dimer concentration and decreased OH-proline levels, too. Treatment with PTX3 −/− -MSCs ameliorated oxygenation, W/D, and alveolar TNFα, though to a lesser extent than WT-MSCs. PTX3 −/− -MSCs did not improve lung collapse, neutrophil count, CXCL1, D-dimer, and OH-proline concentrations. The protective effects of WT-MSCs were dampened by lack of endogenous PTX3, too. Conclusions: In acid aspiration acute lung injury, MSCs improve pulmonary function and limit fibrosis by fine-tuning inflammation. The role of PTX3 in determining MSCs' effects might merit further scrutiny.

Intraperitoneal adoptive transfer of mesenchymal stem cells enhances recovery from acid aspiration acute lung injury in mice