Cell and Tissue Research最新文献

The Kupffer cell was first discovered by Karl Wilhelm von Kupffer in 1876, labeling them as "Sternzellen." Since their discovery as the primary macrophages of the liver, researchers have gradually gained an in-depth understanding of the identity, functions, and influential role of Kupffer cells, particularly in infection. It is becoming clear that Kupffer cells perform important tissue-specific functions in homeostasis and disease. Stationary in the sinusoids of the liver, Kupffer cells have a high phagocytic capacity and are adept in clearing the bloodstream of foreign material, toxins, and pathogens. Thus, they are indispensable to host defense and prevent the dissemination of bacteria during infections. To highlight the importance of this cell, this review will explore the history of the Kupffer cell in the context of infection beginning with its discovery to the present day.

Carl C. Speidel (1919) and Ernst Scharrer (1928) were privileged witnesses of the encounter between neurons and hormones, a biological phenomenon that had been occurring in nature during millions of years of evolution, as Berta Scharrer started to unfold since 1935 on. The story of neurosecretion is intimately associated to that of the hypothalamus, such a "marvellous region", as Wolfgang Bargmann (1975) called it. This story started more than two millennia ago. We have made an effort to trace the roots of the discoveries that gave rise to a medical discipline, neuroendocrinology. Our trip to the roots covers a period from the fourth century BC, when an extraordinary Medical School was founded in Alexandria, and extends into the late 1970s of the twentieth century, when neuroendocrine research had started to grow exponentially. An effort has been made to track back the origin of each piece of knowledge that was constructing, brick upon brick, the building of this new medical science, hoping that it would help neuroendocrinologists of the new era to find their own roots, to meet their ancestors. Tracking the roots of a particular phenomenon provides the opportunity to have an overview of the whole phenomenon, allowing comprehension rather than merely knowledge. An important purpose pursued throughout this article was to pay a tribute to all those who, in the early days, contributed to the brain-endocrine encounter. We have tried our best to bring back the achievements of most of them.

One hundred years ago, Cell and Tissue Research was founded under the title "Zeitschrift für Zellen- und Gewebelehre," later "Zeitschrift für Zellforschung und mikroskopische Anatomie." The founders were four eminent German and Swiss cell biologists and zoologists, R. Goldschmidt, W. von Möllendorff, H. Bauer, and J. Seiler.

Hieroglyphus banian (H. banian) is a grasshopper species, endemic to South Asia. The optic lobe in Acrididae has been characterized to a great extent in orthoptera, predominantly using Locust species like Schistocerca gregaria, Schistocerca americana, and Locusta migratoria, which are closely related to each other. In this work, we characterize the anatomical features of the optic lobe and associated pathway in the grasshopper species H. banian using tract tracing, immunohistochemistry, and intracellular fills. All the areas of the visual pathways that have been reported in the other orthoptera species could be identified in H. banian. Visual pathways exhibited similar structure and connectivity as shown in immunohistochemistry and tract-tracing results supporting the conservation of these features across species within Acrididae. Two new structures in the posterior protocerebrum, PS1 and PS2 with prominent innervations from the optic lobe were identified. Novel structure PS1 is innervated from medulla via PS1T and, PS2 from aMe via PS2T, both new tracts we have identified.

Limb injuries such as severe strains, deep cuts, gunshot wounds, and ischemia can cause peripheral nerve damage. This can result in a range of clinical symptoms including sensory deficits, limb paralysis and atrophy, neuralgia, and sweating abnormalities in the innervated areas affected by the damaged nerves. These symptoms can have a significant impact on patients' daily lives and work. Despite existing clinical treatments, some patients cannot achieve satisfactory therapeutic effects and continue to experience persistent paralysis and pain. Schwann cells are responsible for repairing and regenerating damaged nerves in the peripheral nervous system. They play a crucial role in the healing of nerve injuries and are essential for the restoration of proper nerve function. An increasing number of studies have focused on the various regulatory mechanisms that specifically affect the repair of damage by Schwann cells. This article aims to provide information on the different types of peripheral nerve injuries and their available treatments. We also discuss the various molecular mechanisms that regulate Schwann cell function during peripheral nerve repair and how they can be used to promote nerve repair and regeneration. Furthermore, we explore the potential therapeutic applications of precision regulation of Schwann cells for the treatment of peripheral nerve injuries.

The mechanisms by which severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) causes severe lung inflammation and mortality remain unclear. While the role of alveolar macrophages in COVID-19 is known, data on pulmonary intravascular macrophages (PIMs) is lacking. PIMs are key inflammatory cells present in species like cattle and pigs. Though constitutively absent in humans and rodents, their recruitment in rodents triggers exaggerated inflammation. We investigated the recruitment of PIMs and other immune cells, using immunofluorescence, hematoxylin and eosin (H&E) staining, and immunogold labeling in a hamster model of SARS-CoV-2 infection. Syrian golden hamsters were divided into 6 groups: uninfected control, unvaccinated-infected at 2-, 5-, and 14-days post infection (dpi) and vaccinated-infected at 5- and 14-dpi. Lung tissues were analyzed for neutrophils (myeloperoxidase), monocytes/macrophages (CCR2, CX3CR1), macrophages (IBA-1), and T cells (CD3). Septal macrophages increased at 2-, 5-, and 14-dpi in infected animals vs. control. CX3CR1 + cells decreased at 14-dpi in unvaccinated animals, but CX3CR1/CCR2 double positive cells were higher at 5-dpi, indicating a pro-inflammatory macrophage phenotype. PIMs were confirmed by transmission electron microscopy. These are the first data showing recruitment of pro-inflammatory PIMs in SARS-CoV-2 infected lungs.

Airway smooth muscle (ASM) dysfunction is a key factor in the narrowing of airways in asthma patients, characterized by excessive secretion of inflammatory factors, increased mass, and amplified contractile responses. These pathological features are instrumental in the propagation of airway inflammation, structural remodeling, and the escalation of airway hyperresponsiveness (AHR), which are also principal factors underlying the limitations of current therapeutic strategies. In asthmatic ASM, an imbalance between oxidant production and antioxidant defenses culminates in oxidative stress, which is involved in the excessive secretion of inflammatory factors, increased mass, and amplified contractile responses of ASM, and is a critical etiological factor implicated in the dysregulation of ASM function. The molecular pathways through which oxidative stress exerts its effects on ASM in asthma are multifaceted, with the Nrf2/HO-1, MAPK, and PI3K/Akt pathways being particularly noteworthy. These characteristic pathways play a potential role by connecting with different upstream and downstream signaling molecules and are involved in the amplification of ASM inflammatory responses, increased mass, and AHR. This review provides a comprehensive synthesis of the phenotypic expression of ASM dysfunction in asthma, the interplay between oxidants and antioxidants, and the evidence base and molecular underpinnings linking oxidative stress to ASM dysfunction. Given the profound implications of ASM dysfunction on the airflow limitation in asthma and the seminal role of oxidative stress in this process, a deeper exploration of these mechanisms is essential for unraveling the pathogenesis of asthma and may offer novel perspectives for its prophylaxis and management.

The smoky brown cockroach, Periplaneta fuliginosa, is a peridomestic pest inhabiting broad regions of the world from temperate to subtropical zones. In common with other related species such as the American cockroach, Periplaneta americana, female-emitted sex pheromone components, named periplanones, are known to be key volatiles that elicit long-range attraction and courtship rituals in males. How periplanones are processed in the nervous system has been entirely unexplored in P. fuliginosa. By using pheromone compounds, periplanones A, B, C, and D, as stimulants to the antenna, we identified four distinct types of interneurons (projection neurons) that relay pheromonal signals from a single olfactory glomerulus of the first-order olfactory center (antennal lobe) to higher-order centers in the ipsilateral hemibrain. All glomeruli innervated by pheromone-responsive projection neurons clustered near the antennal nerve entrance of the antennal lobe. The projection neuron with dendrites in the largest glomerulus was tuned specifically to periplanone-D, and adding other components to periplanone-D counteracted the excitation elicited by periplanone-D alone. Likewise, the projection neuron with dendrites in the second largest glomerulus and that with dendrites in a medium-sized glomerulus were tuned to periplanone-A and periplanone-B, respectively. Our results are, therefore, consistent with behavioral findings that periplanone-D alone acts as a primary sex attractant and that other components act as potential behavioral antagonists. Moreover, a comparison of the glomeruli in P. fuliginosa and P. americana suggested that there are differences in the sizes of homologous glomeruli, as well as in the ligands they process.