We found that, in guinea pig airway smooth muscle, the pharmacological inhibition of RTKs significantly decreased the contraction induced by 20 mM KCl. We observed that MEK pharmacological inhibitors diminished the contraction induced by 20 mM KCl, but not that induced by 60 mM. On the other hand, ERK inhibitors also altered the contraction generated by 20 mM KCl. When a ROCK inhibitor was tested, we found that it significantly inhibited the KCl-induced contraction. These results were complemented with Western blot experiments, and a decrease in ERK phosphorylation was noticed when the RTKs were inhibited. When MEK and ERK inhibitors were used, we also observed a decrease in ERK phosphorylation. In the case of MYPT1, its phosphorylation decreased when RTK, MEK, and ROCK inhibitors were used. In conclusion, we found that, in guinea pig airway smooth muscle, the contraction induced by 20 mM KCl includes the activation of RTKs and, in turn, MEK-ERK and ROCK.

We found that, in guinea pig airway smooth muscle, the pharmacological inhibition of RTKs significantly decreased the contraction induced by 20 mM KCl. We observed that MEK pharmacological inhibitors also diminished the contraction. On the other hand, an ERK or a MLCK inhibitor did not alter the contraction generated by 20 mM KCl. When a ROCK inhibitor was tested, we found that it also significantly inhibited the KCl-induced contraction. These results were complemented with Western blot experiments, and a de-crease in ERK phosphorylation was noticed when the RTKs were inhibited. When MEK and ERK inhibitors were used, we observed a decrease in ERK phosphorylation only. In the case of MYPT1, its phosphorylation decreased when RTKs, MEK and ROCK inhibitors were used. In conclusion, we found that, in guinea pig airway smooth muscle, the con-traction induced by 20 mM KCl includes the activation of RTKs and in turn the MEK and ROCK kinases.

This chapter examines the interaction between dengue virus infection and mucosal involvement. It describes the innate and adaptive immune responses that occur on these surfaces, including the role of epithelial barriers, immune cells, cytokines, and antibody-mediated immunity. Additionally, it reviews the main signaling pathways activated during dengue infection, including their contribution to both the control of viral replication and inflammatory and pathogenic processes. Particular attention is given to the mechanisms through which the immune response can control viral infection, while an excessive or dysregulated response may contibute to tissue damage and disease porgession. Findings from in vitro studies are presented, and clinical cases are analyzed, reporting the clinical manifestations observed in the oral, nasal, conjunctival, and genital mucosa, with special emphasis on identifying warning signs in patients with dengue infection. These manifestations are discussed in relation to the systemic effects of dengue and their potential clinical relevance. Furthermore, a comparison is made with other infections caused by arboviruses, such as Zika and Chikungunya viruses, to identify similarities and differences in mucosal involvement and facilitate differential diagnosis. This comparison also provides a broader understanding of the clinical manifestations associated with arboviral infections and their importance in patient evaluation.Finally, potential therapeutic strategies aimed at modulating the immune response and mitigating disease progression are discussed. This chapter emphasizes continued research into pharmacological treatments and therapeutic strategies to reduce inflammation, control viral replication, and prevent tissue damage, while recognizing dengue is mucosal effects and clinical features to enable early diagnosis and timely tretament.