Ellen Dyminski Parente Ribeiro

Leishmaniasis is a neglected tropical disease with high global health and socioeconomic burden, particularly in low‐income regions where current treatments remain limited by high toxicity, cost, and increasing resistance. Antimicrobial peptides (AMPs), small bioactive molecules with broad‐spectrum activity and low propensity for resistance, have emerged as promising therapeutic candidates. This scoping review aimed to map the existing literature on AMPs with anti‐leishmanial activity, updating and expanding upon previous reviews. Following the PRISMA‐ScR framework, we systematically searched for primary research articles assessing natural and synthetic peptides through in vitro or in vivo approaches. Seventy‐nine studies met eligibility criteria, evaluating 231 unique peptides against multiple Leishmania species. Most investigations were in vitro, particularly on L. major promastigotes and amastigotes. Synthetic and bioengineered peptides demonstrated superior efficacy and selectivity compared with natural peptides, in some cases achieving selectivity indices exceeding 6000. Mechanistic studies revealed that AMPs act primarily through parasite membrane disruption, but also by inducing apoptosis‐like processes and modulating host immune responses. Despite their promise, several challenges remain, including peptide instability in physiological conditions, proteolytic degradation, and limited in vivo validation. Advances in chemical modifications and nanocarrier‐based delivery systems show potential to overcome these barriers. In conclusion, AMPs represent a compelling avenue for leishmaniasis therapy, especially for cutaneous forms of the disease. However, further studies, particularly in vivo, are critical to translate preclinical findings into clinical application.

Infrasound, physically defined as sound at frequencies below 20 Hertz, can travel long distances with minimal attenuation and permeate biological tissues due to its marked particle displacement and deep penetration. Generated by both natural phenomena and human-made systems, infrasound has drawn increasing scientific and public attention regarding its potential physiological and psychological effects. Experimental studies demonstrate that infrasound can modulate mechanosensitive structures at the cellular level, particularly pressure-sensitive ion channels such as PIEZO1 and TRPV4, leading to intracellular calcium influx, oxidative stress, altered intercellular communication, and in some settings, apoptosis. These responses vary according to sound pressure levels, frequencies, exposure duration, and tissue type. In the cardiovascular system, higher sound pressures have been associated with mitochondrial injury and fibrosis, whereas low sound pressures may exert context-dependent protective effects. In animal models, prolonged or intense exposure to infrasound has been shown to induce neuroinflammatory responses and memory impairment. Short-term studies in humans at moderate intensities have reported minimal physiological changes, with psychological and contextual factors influencing symptom perception. Occupational environments such as factories and agricultural settings may contain elevated levels of infrasound, underscoring the importance of systematic measurements and exposure assessments. At the same time, controlled infrasound stimulation has shown potential as an adjunct modality in bone repair and tissue regeneration, highlighting its dual capacity as both a biological stressor and a possible therapeutic tool. Overall, existing data indicate that infrasound may be harmful at chronic exposure depending on intensity and frequency, yet beneficial when precisely regulated. Future research should standardize exposure metrics, refine measurement technologies, and clarify dose–response relationships to better define the health risks and therapeutic applications of infrasound.

Infrasound, physically defined as sound at frequencies below 20 Hertz, can travel long distances with minimal attenuation and permeate biological tissues due to its marked particle displacement and deep penetration. Generated by both natural phenomena and human-made systems, infrasound has drawn increasing scientific and public attention regarding its potential physiological and psychological effects. Experimental studies demonstrate that infrasound can modulate mechanosensitive structures at the cellular level, particularly pressure-sensitive ion channels such as PIEZO1 and TRPV4, leading to intracellular calcium influx, oxidative stress, altered intercellular communication, and in some settings, apoptosis. These responses vary according to sound pressure levels, frequencies, exposure duration and tissue type. In the cardiovascular system, higher sound pressures have been associated with mitochondrial injury and fibrosis, whereas low sound pressures may exert context-dependent protective effects. In animal models, prolonged or intense exposure to infrasound has been shown to induce neuroinflammatory responses and memory impairment. Short-term studies in humans at moderate intensities have reported minimal physiological changes, with psychological and contextual factors influencing symptom perception. Occupational environments such as factories and agricultural settings may contain elevated levels of infrasound, underscoring the importance of systematic measurements and exposure assessments. At the same time, controlled infrasound stimulation has shown potential as an adjunct modality in bone repair and tissue regeneration, highlighting its dual capacity as both a biological stressor and a possible therapeutic tool. Overall, existing data indicate that infrasound may be harmful at chronic exposure depending on intensity and frequency, yet beneficial when precisely regulated. Future research should standardize exposure metrics, refine measurement technologies, and clarify dose–response relationships to better define the health risks and therapeutic applications of infrasound.

Sepsis causes profound microcirculatory dysfunction, where heterogeneous capillary perfusion and abnormal vasomotion contribute to tissue hypoxia and organ failure. Sublingual videomicroscopy is established in large animals and humans to monitor these alterations, but this approach has not been applied in murine models. We developed a method to assess sublingual perfusion and vasomotion in mice using sidestream dark field (SDF) videomicroscopy. Male C57BL/6 mice were anesthetized, and sublingual vessels were imaged for 90 min. Perfusion and vasomotion parameters were assessed, and a Fast Fourier Transform was performed on vasomotion data to characterize the frequency components of rhythmic microvessel diameter changes. Another group of animals was administered lipopolysaccharide (LPS) intraperitoneally as a model of systemic inflammation in sepsis. LPS-treated mice exhibited a significant decline in the proportion of perfused vessels at 90 min and in the microvascular flow index. Very low-frequency vasomotion (0.005–0.15 Hz) declined in controls but was preserved during endotoxemia, suggesting an active microvascular tone response to inflammatory stress. This study establishes the first murine protocol for sublingual SDF imaging, allowing early detection of perfusion deficits and vasomotor changes in experimental sepsis. The minimal-invasive approach offers a translational platform for mechanistic and therapeutic studies in sepsis.

Sepsis causes profound microcirculatory dysfunction, where heterogeneous capillary perfusion and abnormal vasomotion contribute to tissue hypoxia and organ failure. Sublingual videomicroscopy is established in large animals and humans to monitor these alterations, but this approach has not been applied in murine models. We developed a method to assess sublingual perfusion and vasomotion in mice using sidestream dark field (SDF) videomicroscopy. Male C57BL/6 mice were anesthetized, and sublingual vessels were imaged for 90 minutes. Perfusion and vasomotion parameters were assessed, and a Fast Fourier Transform was performed on vasomotion data to characterize the frequency components of rhythmic microvessel diameter changes. Another group of animals was administered lipopolysaccharide (LPS) intraperitoneally as a model of systemic inflammation in sepsis. LPS-treated mice exhibited a significant decline in the proportion of perfused vessels at 90 minutes and in the microvascular flow index. Very low-frequency vasomotion (0.005–0.15 Hz) declined in controls but was preserved during endotoxemia, suggesting an active microvascular tone response to inflammatory stress. This study establishes the first murine protocol for sublingual SDF imaging, allowing early detection of perfusion deficits and vasomotor changes in experimental sepsis. The minimal-invasive approach offers a translational platform for mechanistic and therapeutic studies in sepsis.