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The first quantitative studies of pulmonary and cutaneous respiration in the amphibians were made on Rana esculenta and Rana temporaria by Krogh (1904). He inserted a cannula connected to an air pump into the trachea and analyzed separately the air forced through the lungs by the pump and the air surrounding the frog. He was able to show that in R. temporaria the lungs and skin are both important in respiratory exchange but in somewhat different ways. Oxygen enters through the lungs whereas carbon dioxide is excreted through the skin. Oxygen intake through the skin is determined solely by physical limitation while carbon dioxide excretion may vary with environmental charges. Krogh concluded that in R. temporaria the lungs dominate in oxygen consumption over the skin in a ratio of 3:1. In R. esculenta the ratio was 1:1. This probably correlated with the more aquatic habitat of R. esculenta. In the salamander, Ambystoma maculatum, Hutchison (1963) found that not only is eighty percent of the carbon dioxide produced released through the skin but the skin is also responsible for more than fifty percent of the total oxygen uptake at 15°C and below. Rana catesbeiana tadpoles were used in these experiments. They were obtained from the Mokelumne River on Highway 88, two miles west of Clements, California The function of the lungs in Rana catesbeiana tadpoles was studied.

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Bronchopulmonary dysplasia (BPD), the chronic lung disease that develops in premature babies following mechanical ventilation and oxygen exposure, is the most common complication of extreme prematurity. Currently, there is no cure for BPD. Increasing evidence indicates early-onset emphysema and pulmonary vascular disease in survivors with BPD (Aukland et al., 2006; Wong et al., 2008), suggesting an irreversible arrest in lung growth and/or premature lung aging resulting in life-long health problems (J. Sucre et al., 2021). Transient in vivo cellular reprogramming through the activation of the Yamanaka reprogramming factors Oct4, Sox2, Klf4, c-Myc (OSKM), ameliorate cellular and physiological hallmarks of aging and to promote tissue regeneration and improve organ function after injury. (Chen et al., 2021a; Hishida et al., 2022b; Lu et al., 2020) This thesis focuses on determining if transient in vivo cellular reprogramming can regenerate an established lung injury in a BPD mouse model. Two strategies, (a) Adeno-Associated virus (AAV) mediated transient overexpression of the OSK factors and (b) using a transgenic reprogrammable mouse line to overexpress the OSKM factors were employed to test the efficiency of in vivo cellular reprogramming in regenerating the lungs. Both the strategies, under the conditions tested, did not regenerate established lung injury in a BPD mouse model but the feasibility of both these strategies was established here laying a foundation for the next phase of the study.

As lower respiratory infections are a leading cause of morbidity and mortality worldwide, and have been linked to periodic pandemics, there is a heightened interest in understanding how protective immune cells are mobilized in response to pathogens and contribute to local tissue resistance. The existence of non-recirculating lung resident memory B (BRM) cells was recently defined in an influenza virus infection model and inferred to be protective. Our body of knowledge has since grown significantly, but many unknowns including BRM cell establishment dynamics and requirements for maintenance remain. We previously used a murine model of serotype-independent immunity against Streptococcus pneumoniae (Sp) to show that resident memory B (BRM) cells are seeded extravascularly in the lung after local bacterial exposures independently of mature tertiary lymphoid structure formation. Using a transgenic mouse model which allowed for the depletion of PD-L2+ memory B cells, we demonstrated that lung PD-L2+ BRM cells directly contribute to clearance of a heterotypic Sp challenge infection, and that their absence correlated with diminished local antibody secreting cell (ASC) activities. Our findings provide evidence of serotype-independent protection mediated by the PD-L2+ BRM cell population and suggest that this is due to their capacity to rapidly differentiate into local ASCs upon memory recall. We carried out additional studies to elucidate lung B cell population dynamics, locations, and T-dependent requirements for establishment and maintenance after Sp infections. Singular exposure to self-limiting pneumococcal infection was insufficient to generate lasting BRM cells, as well as other heterogeneous extravascular B cell populations which were tracked over time. This included a transient population of proliferatively active lung GC B cells whose accumulation in the lung corresponded with the temporary appearance of organized lymphoid tissue. After an initial respiratory infection was administered to allow for immune priming in the lung and in draining lymph nodes, disruption of T cell interactions during a 2nd infection prevented pan extravascular B cell accumulation and abrogated lung BRM cells. We posit that our findings are relevant for the development of improved serotype-independent preventative strategies against pneumococcal pneumonia, and all respiratory pathogens in general. Advancing our understanding of tissue-resident B cell populations will aid in the development of next generation vaccines that leverage mucosal memory against respiratory pathogens. / 2025-02-12T00:00:00Z