The structure of the human gut microbial community is determined by host genetics and environmental factors, where alterations in its structure have been associated with the onset of different diseases. Establishing a defined human gut microbial community within inbred rodent models provides a means to study microbial-related pathologies, however, an in-depth comparison of the established human gut microbiota in the different models is lacking. We compared the efficiency of establishing the bacterial component of a defined human microbial community within germ-free (GF) rats, GF mice, and antibiotic-treated specific pathogen-free mice. Remarkable differences were observed between the different rodent models. While the majority of abundant human-donor bacterial phylotypes were established in the GF rats, only a subset was present in the GF mice. Despite the fact that members of the phylum Bacteriodetes were well established in all rodent models, mice enriched for phylotypes related to species of Bacteroides. In contrary to the efficiency of Clostridiales to populate the GF rat in relative proportions to that of the human-donor, members of Clostridia cluster IV only poorly colonize the mouse gut. Thus, the genetic background of the different recipient rodent systems (that is, rats and mice) strongly influences the nature of the populating human gut microbiota, determining each model's biological suitability.

The IDDM (LEW.1AR1/Ztm-iddm) rat is a type 1 diabetic animal model characterized by a rapid apoptotic pancreatic ␤-cell destruction. Here we have analyzed the time course of islet infiltration, changes in the cytokine expression pattern, and ␤-cell apoptosis in the transition from the pre-diabetic to the diabetic state. Transition from normoglycemia to hyperglycemia occurred when ␤-cell loss exceeded 60 -70%. At the early stages of islet infiltration, macrophages were the predominant immune cell type in the peripherally infiltrated islets. Progression of ␤-cell loss was closely linked to a severe infiltration of the whole islet by CD8 T ype 1 diabetes is an autoimmune disease leading, after a pre-diabetic period, to overt diabetes due to destruction of the pancreatic ␤-cells (1-3). Despite many efforts, the mechanisms of interaction between the infiltrating immune cells in the pancreatic islets and pancreatic ␤-cell death, which finally causes insulin-dependent diabetes, are not well understood (1-3). The pre-diabetic period is of special interest for understanding the mechanisms responsible for pancreatic ␤-cell destruction. Animal models of human type 1 diabetes can provide an important contribution to a better understanding of the etiopathology underlying apoptotic ␤-cell death in type 1 diabetes. The IDDM (LEW.1AR1/Ztm-iddm) rat is a new, particularly attractive autoimmune diabetes animal model (4) for the analysis of the different stages of the immune cell infiltration process because of the short normoglycemic pre-diabetic period with pancreatic islet infiltration of ϳ1 week before ending in a state of overt hyperglycemia due to apoptotic ␤-cell destruction (4,5). In contrast to the bio-breeding (BB) rat and the nonobese diabetic (NOD) mouse as the most studied rodent models, the IDDM rat closely resembles the diabetic syndrome in humans because the animals show a fully developed cellular immune system and no sex bias in diabetes incidence (4,5). In this study, the process of immune cell infiltration in the islets of the pancreas of littermates originating from a homozygous pairing of diabetic parents was investigated. The results allow us to delineate the sequence of pathological changes leading to apoptotic ␤-cell death in this animal model of human type 1 diabetes. RESEARCH DESIGN AND METHODSLEW.1AR1/Ztm-iddm rats were housed in the Institute of Laboratory Animal Science of Hannover Medical School as described previously (4). The animals originated from a breeding colony (4) that was maintained through mating of diabetic female and diabetic male IDDM rats (F7; seventh generation of the IDDM rat; see http://www.mh-hannover.de/institute/clinbiochemistry/iddmrat. htm for details). Homozygous pairing with both parents diabetic resulted in a diabetes incidence of ϳ60%. All rats were maintained according to the FELASA (Federation of European Laboratory Animal Science Associations) guidelines. The animals were investigated at days 45, 50, 55, 59, 60, or 65 after birth. On the day the animals were killed, tissu...

The proliferation of vascular smooth muscle cells is controlled by specific growth factors and cytokines acting in paracrine networks. Macrophage products such as the platelet-derived growth factor and interleukin 1 promote smooth muscle proliferation and are released in the arterial wall during atherosclerosis and repair processes. T lymphocytes are also present in vascular tissue, but their role in vascular growth control in vivo has been unclear. We now demonstrate that rats in which T lymphocytes have been eliminated by a monoclonal antibody develop larger proliferative arterial lesions after balloon-catheter injury. Larger lesions also develop in athymic rnu/rnu rats that lack T lymphocytes, when compared with rnu/+ littermates with normal T-cell levels. Finally, injection of the lymphokine interferon y inhibits smooth muscle proliferation and results in smaller lesions compared with controls injected with buffer alone. These results indicate that T lymphocytes modulate smooth muscle proliferation during vascular repair. We propose that T lymphocytes may play an important, immunologically nonspecific role in tissue repair processes.The proliferation of vascular smooth muscle cells (SMC) is controlled by specific growth factors and cytokines acting in paracrine networks (1-4). It was previously thought that the major growth-regulating factors were released by platelets adhering to deendothelialized arterial surfaces, but inflammatory cells may be equally important as growth regulators for SMC (2-4).Macrophage products, such as the platelet-derived growth factor and interleukin 1, promote SMC proliferation in cell culture (1,2,5,6) and are expressed in the arterial wall during atherosclerosis and repair processes after experimental injury (7-10). T lymphocytes are also present in vascular tissue during atherosclerosis and vascular repair (3,(11)(12)(13)(14), but their role in vascular growth control in vivo has been unclear. We have previously found that the T-lymphocyte product interferon y (IFN-'y) inhibits SMC proliferation (15, 16); this finding would point toward a growth-inhibitory role of T lymphocytes in vascular repair. It was, however, also found that the immunosuppressive drug cyclosporin A inhibits development of a proliferative lesion after injury to rat arteries, which could imply a growth-promoting effect of T cells (17). Whether T cells promote or inhibit SMC proliferation in vivo was, therefore, unclear. We have now attempted to determine the role of T lymphocytes in the vascular response to injury in vivo by using T-cell-deficient rats.Proliferation of SMC can be studied in vivo by using a catheter to remove the endothelial lining of a carotid artery segment in the rat. This procedure results in SMC migration from the medial to intimal layer of the artery, SMC proliferation in the intima, and formation of an intimal lesion that reduces the size of the arterial lumen (18). The lesions are dominated by SMC, but a few monocyte-derived macrophages and T lymphocytes are also present (13)....

With the exception of the Komeda rat, the animal models mirror very well the situation in humans with type 1 diabetes. Thus animal models of type 1 diabetes can provide meaningful information on the disease processes in the pancreas of patients with type 1 diabetes.

IntroductionHuman speech does not only communicate linguistic information but also paralinguistic features, e.g. information about the identity and the arousal state of the sender. Comparable morphological and physiological constraints on vocal production in mammals suggest the existence of commonalities encoding sender-identity and the arousal state of a sender across mammals. To explore this hypothesis and to investigate whether specific acoustic parameters encode for sender-identity while others encode for arousal, we studied infants of the domestic cat (Felis silvestris catus). Kittens are an excellent model for analysing vocal correlates of sender-identity and arousal. They strongly depend on the care of their mother. Thus, the acoustical conveyance of sender-identity and arousal may be important for their survival.ResultsWe recorded calls of 18 kittens in an experimentally-induced separation paradigm, where kittens were spatially separated from their mother and siblings. In the Low arousal condition, infants were just separated without any manipulation. In the High arousal condition infants were handled by the experimenter. Multi-parametric sound analyses revealed that kitten isolation calls are individually distinct and differ between the Low and High arousal conditions. Our results suggested that source- and filter-related parameters are important for encoding sender-identity, whereas time-, source- and tonality-related parameters are important for encoding arousal.ConclusionComparable findings in other mammalian lineages provide evidence for commonalities in non-verbal cues encoding sender-identity and arousal across mammals comparable to paralinguistic cues in humans. This favours the establishment of general concepts for voice recognition and emotions in humans and animals.