Number Of Lymphoid Follicles Research Articles

Alterações histológicas da pars esophagea de suínos e sua relação com Helicobacter spp.

A relação entre Helicobacter spp. e a presença de alterações histológicas na pars esophagea de suínos foi avaliada em 67 estômagos de animais em idade de abate. Para a identificação das helicobactérias, utilizou-se a técnica da PCR com primers específicos para o gênero Helicobacter. As alterações histológicas foram identificadas e classificadas como ulceração, erosão, degeneração epitelial, alongamento de papilas, hiperplasia, paraqueratose, intensidade do infiltrado inflamatório e aumento do número de folículos linfoides. As alterações mais frequentemente encontradas na pars esophagea foram a degeneração epitelial e o alongamento de papilas, observadas em 83,5% (n=56) das amostras analisadas. Em 77,5% (n=52) das amostras, observou-se paraqueratose e em 61,1% (n=41) hiperplasia epitelial. Quarenta e sete (70,1%) foram positivas na PCR para Helicobacter spp. Nessas amostras a erosão foi a lesão mais observada (40,2%), seguida de ulceração da mucosa (11,9%). Em 58,2% das amostras positivas na PCR, não foram observadas ulcerações de mucosa. Observou-se associação significativa (P=0,003) entre a presença de Helicobacter spp. e a degeneração epitelial da pars esophagea de suínos em idade de abate.

Helicobacter pylori eradication improves gastric histology and decreases serum gastrin, pepsinogen I and pepsinogen II levels in patients with duodenal ulcer

The aim of this study was to assess the gastric histopathology and serum gastrin-17 and pepsinogens profiles in patients with duodenal ulcer before and after Helicobacter pylori eradication in a population with a very high prevalence of H. pylori. At the same time we assessed the role of H. pylori density on these variables. Eighty Caucasian patients with H. pylori-associated duodenal ulcer before treatment and 1 year after randomized eradication were studied. Among patients with unsuccessful eradication two groups were distinguished according to the data obtained after treatment: the group with negative rapid urease test and decreased bacterial density according to morphological score (partial elimination group); the group with positive rapid urease test and high bacterial density (failed eradication group). One year after successful eradication, serum levels of gastrin-17, pepsinogen I and pepsinogen II decreased. Similar changes of serum pepsinogen I and pepsinogen II levels were observed in patients with partial elimination of H. pylori infection. In the group with successful eradication, inflammation, activity, atrophy and number of lymphoid follicles in the antral mucosa fell. In the group with partial elimination, antral mucosa activity and H. pylori score reduced. Other morphological changes were statistically non-significant. Patients with duodenal ulcer after successful eradication have improvement of morphological and functional characteristics of gastric mucosa.

Treatment of chronic idiopathic large-bowel diarrhea in dogs with a highly digestible diet and soluble fiber: a retrospective review of 37 cases.

The medical records of 37 dogs diagnosed with chronic idiopathic large-bowel diarrhea were reviewed. The median age of affected dogs was 6 years. The median body weight was 13.9 kg. The median duration of clinical signs before diagnosis was 32 weeks. Diarrhea usually was intermittent and characterized by increasing frequency, fecal mucus, hematochezia, and tenesmus. Vomiting was common but usually much less frequent and severe than the diarrhea. A variety of stressful factors and abnormal personality traits were identified. CBC and serum biochemistry usually were normal. Fecal examination rarely identified parasites. Rectal cytology specimens were most often normal, but some dogs had increased numbers of neutrophils. The colonic mucosa often was normal during colonoscopy, but decreased numbers of lymphoid follicles were found in some dogs. Histopathologic evaluation found that colonic mucosa was within normal limits. Treatment with soluble fiber (Metamucil) added to a highly digestible diet (Hills i/d) resulted in a very good to excellent response in most dogs. The median initial dosage of Metamucil was 2 tablespoons (2 T) per day. In some dogs, the fiber dosage was reduced or eliminated, or a grocery store brand of dog food was substituted, without causing diarrhea to return.

Large Intestine Histopathology of Pegylated-Interferon-Alpha Plus Ribavirin Treated Chronic Hepatitis C Patients

Large Intestine Histopathology of Pegylated-Interferon-Alpha Plus Ribavirin Treated Chronic Hepatitis C Patients

The Bak protein expression in germinal centers of hypertrophied adenoids in children

The aim of this study was to evaluate pro-apoptotic Bak expression in the germinal centers of adenoid in children on the assumption of the potential usefulness of Bak as adenoid function marker. The study involved 95 children undergoing adenoidectomy; divided into three age groups: aged up to 5 years (25 children), 5-10 years (54 children) and over 10 years (16 children). The analyzed material was adenoids removed on the ground of hypertrophy. Immunohistochemical analyses were carried out using goat polyclonal Bak antibodies (DAKO) directed against human Bak protein. The presence of Bak positive lymphocytes within germinal centers and Bak immunostaining were scored. The immunohistochemical staining showed the Bak positive lymphocytes mainly within the germinal centers of the lymphoid follicles. The Bak reactivity was also present in hyperplastic lymphoid tissue within the subepithelial B lymphocytes. We have not found statistically significant correlation between Bak expression and clinical status and change in Bak expression level according to age. The apoptotic presence within the germinal centers are the manifestation of which is Bak expression and its lack in the mantle zone, what we confirmed in our former study by describing Bcl-2 expression, seems to be a proper B cells maturation marker within lymphoid follicles. Our finding shows that these processes are not influenced by age and supports our thesis that adenoid involution is rather the effect of changes in the number of lymphoid follicles that changes in them.

Helicobacter pylori Gastritis in Children Is Associated With a Regulatory T-Cell Response

Helicobacter pylori infection in children infrequently causes gastroduodenal mucosal ulceration. Because H pylori induces T-cell dependent gastric inflammation in adults and T regulatory (Treg) cells suppress T-cell-dependent pathology, we evaluated gastric histopathology and Treg cell responses in H pylori-infected children and adults. Gastric tissue from 36 children and 79 adults with abdominal symptoms in Santiago, Chile, was evaluated prospectively for H pylori bacteria and histopathology using the Sydney classification and Treg responses using immunoassay, immunohistochemistry, and real-time polymerase chain reaction. Eighteen (50%) of the children and 51 (65%) of the adults were infected with H pylori. Children and adults were colonized with similar levels of H pylori. However, the level of gastritis in the children was reduced substantially compared with that of the adults (P < .05). Coincident with reduced gastric inflammation, the number of Treg cells and levels of Treg cytokines (transforming growth factor [TGF]-beta1 and interleukin-10) were increased markedly in the gastric mucosa of H pylori-infected children compared with that of infected adults (P < .03 and < .05, respectively). Also, H pylori infection in the children was associated with markedly increased levels of gastric TGF-beta1 and interleukin-10 messenger RNA. Importantly, gastric TGF-beta1 in H pylori-infected children localized predominantly to mucosal CD25(+) and Foxp3(+) cells, indicating a Treg source for the TGF-beta1. Gastric pathology is reduced and local Treg cell responses are increased in H pylori-infected children compared with infected adults, suggesting that gastric Treg cell responses down-regulate the inflammation and ulceration induced by H pylori in children.

INDUCTION OF ANTIGEN-DEPENDENT EOSINOPHILIC INFLAMMATION IN THE COLON BY LOCAL TRANSFER OF CONVENTIONAL ANTIGEN IN TH2-SENSITIZED MICE

Colon eosinophilic inflammation is featured in a variety of gastrointestinal disorders including eosinophil-associated gastrointestinal disorder (EGID), allergy, inflammatory bowel disease, and parasite infection. We hypothesize that a possible immunological mechanism for gastrointestinal eosinophilia is induction by an antigen in a host that is associated with Th2-skewed antigen-specific immune responses. To investigate this, we maintained BALB/c mice under pathogen-free conditions and sensitized them with conventional antigen ovalbumin in conjunction with aluminum hydroxide. After sensitization, the animals developed polarized Th2 type responses to the same antigen seen in both systemic and local mucosal compartments. Seven days later mice were challenged at the colonic mucosa, by intrarectal administration, with ovalbumin encoded in an adenoviral vector. After mucosal challenge, preconditioned animals developed significant colonic inflammation, characterized by the presence of enlarged and increases in number of lymphoid follicles, and marked eosinophilic infiltration. These pathogenic changes peaked at day 5, but resolved by day 10-15, at which time local antigen expression diminished. The colonic epithelium was found integrated; no epithelial cell damage detected through the entire course. Local antigen expression was not found different between sensitized and naive mice, the latter of which did not demonstrate inflammation post challenge. We confirmed that sensitized mice did not develop any local immunological or physiological changes if challenged with adenoviral vector that does not contain ovalbumin. In conclusion, we here established a mouse model which may suggest that exposure of the lower gastrointestinal mucosa to a conventional antigen that is associated with Th2-skewed responses preexisted.

Histological changes in the gastric mucosa after Helicobacter pylori eradication.

Correa described a stepwise model of changes in the gastric mucosa after Helicobacter pylori infection, from the normal gastric epithelium to chronic gastritis, atrophy, intestinal metaplasia, dysplasia and adenocarcinoma. The aim of this study is to assess the reversibility of these mucosal changes after H. pylori eradication. The study sample consisted of 89 patients who underwent at least two gastric biopsies from 1990 to 2000, with a positive finding for H. pylori in the first and a negative finding in the second. Specimens were evaluated for acute and chronic inflammation, lymphoid aggregates, proliferation, mucosal atrophy, intestinal metaplasia, dysplasia, and MUC5AC and MUC6 expression using histochemical and immunohistochemical methods. The average time between biopsies was 23.15 +/- 26.30 months. There was a significant decrease in acute and chronic inflammation scores, from 1.48 +/- 1.10 to 0.23 +/- 0.63 and from 2.67 +/- 0.68 to 1.44 +/- 1.04, respectively (P < 0.001), and in a number of lymphoid follicles, from 42.68% to 21.95% of cases (P < 0.008). The number of glands increased from 39.08 +/- 16.67/mm to 48.86 +/- 17.93/mm after eradication (P = 0.062). Intestinal metaplasia was found in 17.07% of the cases, with no change over time. Dysplasia appeared in one case 2 years after eradication. In 27 patients, the Ki67 labeling index decreased significantly after eradication, while MUC5AC and MUC6 expression increased. Our findings, although not conclusive for arrest of the malignant potential, support the importance of H. pylori eradication in the prevention of gastric cancer.

The Bcl-2 protein expression in germinal centers of hypertrophied adenoids in children

The aim of this study was to evaluate Bcl-2 expression in the germinal centers of adenoid in children on the assumption that it can be treated as a marker of adenoidal tissue function. The study involved 95 children. The patients were divided into three age groups: aged up to 5, 5–10 and above 10 years. The analysed material were adenoids removed on the grounds of hypertrophy. Immunohistochemical analyses were carried out using monoclonal antibodies (DAKO/Bcl-2, No. M0887) directed against human Bcl-2 protein. The presence of Bcl-2 positive lymphocytes within the lymphoid follicles and Bcl-2 immunostaining were scored. The immunohistochemical staining showed Bcl-2 positive lymphocytes in the examined sections of adenoidal tissue and their characteristic location, mainly within the mantle zone. Bcl-2 reactivity was widespread in hyperplastic lymphoid tissue, including germinal centers surroundings, scattered cells within the germinal centers and the T-cell areas in general. We have not found statistically significant correlation between Bcl-2 expression and clinical status and change in Bcl-2 expression level according to age. The apoptosis presence within the germinal centers and its lack in mantle zone, the manifestation of which is Bcl-2 expression, is a sign of a proper lymphocytes maturation within lymphoid follicles. It seems that these processes are not influenced by age, so the adenoid involution is probably associated with the changes in the number of lymphoid follicles rather than change or inhibition of the processes that take place in them.

Increase in lymphoid follicles and leukocyte adhesion molecules emphasizes a role for the gut in spondyloarthropathy pathogenesis.

The aim of this study was to investigate the expression of leukocyte adhesion molecules and the number of lymphoid follicles in gut mucosa of patients with spondyloarthropathy (SpA) in comparison with controls, in search for early immune alterations in the development of SpA-related gut inflammation. Histological evaluation and immunohistochemistry were performed on the ileum and colon of 14 SpA patients without macroscopic or microscopic gut inflammation and those of 21 controls. Lymphoid follicles were counted and immunohistochemical staining for leukocyte adhesion molecules, lymphocyte subtypes, macrophages, and plasma cells was scored semi-quantitatively. The number of lymphoid follicles was increased in both the ileum (p < 0.01) and the colon (p < 0.01) of SpA patients. SpA ileum showed an increase in leukocytes expressing CD11c (p < 0.01), whereas CD11a(+) (p < 0.02) and VCAM-1(+) cells (p < 0.05) were increased in SpA colon. Macrophages, characterized by the expression of CD68, were more numerous in colonic mucosa from SpA patients (p < 0.05). The amount of lymphoid follicles and lamina propria mononuclear cells expressing CD11a, CD11c, and VCAM-1 was increased in non-inflamed gut mucosa from SpA patients. These findings might point to increased antigen handling and presentation and augmented maturation of naïve T cells towards memory T cells in the SpA gut, which supports the concept that the gut is involved in the pathogenesis of SpA.

Relevance of VacA and mucosal pathological changes in Chinese patients with upper gastrointestinal diseases before and after Helicobacter pylori eradication

OBJECTIVE: To investigate the influence of VacA activity on gastric mucosa prior to and after Helicobacter pylori eradication in Chinese patients with peptic ulcers and chronic gastritis.METHODS: Seventy‐four dyspeptic patients with H. pylori infection were enrolled. The status of H. pylori infection was evaluated by culture and histo­pathology before and 4−6 weeks after H. pylori eradication therapy. Histological specimens were examined and graded semiquantitatively according to the updated Sydney classification.RESULTS: Helicobacter pylori with VacA was found in 59 of 74 patients (80%), and its prevalence in patients with peptic ulcers and chronic gastritis was similar. Helicobacter pylori eradication rates in patients with VacA+ and VacA− strains were similar. Before eradication, the degrees of acute or chronic inflammation, epithelial damage, atrophy, intestinal metaplasia (IM) and the number of lymphoid follicles were similar in patients with VacA+ and VacA−H. pylori. Four to 6 weeks after the eradication of H. pylori infection, the degrees of acute and chronic inflammation, and epithelial damage in the antrum decreased significantly, particularly in patients with VacA+H. pylori (P &lt; 0.0001). The number of lymphoid follicles in the antrum also decreased more in patients with VacA+H. pylori than in those with VacA−H. pylori (P= 0.051). However, there was no difference in the extent of atrophy and IM between these two groups.CONCLUSIONS: There is no specific correlation between VacA+/VacA−H. pylori strains and mucosal clinicopathological features in Chinese patients with upper gastrointestinal diseases before and after eradication therapy. Successful eradication of H. pylori infection does not improve atrophic and IM lesions of the gastric mucosa.

Antral nodularity and positive CagA serology are distinct and relevant markers of severe gastric inflammation in children with Helicobacter pylori infection.

The aim of this study was to assess whether the endoscopic finding of antral nodularity and serum IgG antibodies to CagA are associated with higher grades of gastric inflammation. The comprehensive data of two previously published trials were reanalysed. One hundred and fifty-three children (median age 9.5 years) who underwent gastroscopy were included. Biopsy specimens from the antrum and corpus were taken to assess Helicobacter pylori status, gastritis score and lymphoid follicles. During endoscopy, antral nodularity was noted. Serum samples were assayed for IgG antibodies to CagA. The presence of antral nodularity (nod+) and positive CagA serology (CagA+) were each found in 32 of the 77 (41.5%) children who had evidence of H. pylori infection. Cross tabulation showed that 20 children (26%) were nod+/CagA+, 12 (15.5%) nod+/CagA-, 12 (15.5%) nod-/CagA+ and 33 (43%) nod-/CagA-. Gastritis score was significantly lower in nod-/CagA- children than in nod+/CagA- (p =.004), nod-/CagA+ (p =.002) and nod+/CagA+ (p <.001), both in the antrum and corpus. Completely normal gastric histology was only found in the nod-/CagA- subgroup of H. pylori-infected children (eight of 33, 24%). Regression analysis showed that antral nodularity and positive CagA serology were related to severe gastric inflammation independently of each other and age. Separate analysis showed that inflammation (p <.001), activity (p <.001) and H. pylori density (p =.002) scores were significantly lower in nod-/CagA- children compared with nod+/CagA+ children. The number of lymphoid follicles in the gastric mucosa was related to antral nodularity (p =.003) and positive CagA serology (p =.043), independently of each other. Antral nodularity and positive CagA serology are distinct and relevant markers of severe gastric inflammation in children with H. pylori infection. The lack of both findings in the same child reflects low-grade or no gastritis.

Helicobacter spp. infection in cats: evaluation of the humoral immune response and prevalence of gastric Helicobacter spp.

The principal aims of this study were to evaluate the humoral immune response (IgG) of cats with gastric Helicobacter spp. infection, and to determine the prevalence of different types of Helicobacter spp. in the stomachs of cats. The Helicobacter infection status of 45 cats (12 healthy spay/neuter cats, 9 sick cats, 24 colony cats) was determined by evaluating endoscopic gastric biopsies for urease activity, presence of Helicobacter-like organisms (HLO) on histopathology, and genus and species-specific PCR. Serum samples were evaluated with a kinetic enzyme linked immunosorbent assay (ELISA) utilizing the high molecular cell-associated protein (HM-CAP) fraction of H. felis ATCC 49179. Seventeen of 45 cats were infected with Helicobacter spp.: “ H. heilmannii” 9/17, H. felis 4/17, mixed “ H. heilmannii” and H. felis 3/17, unclassified- Helicobacter spp. 7/17. H. pylori was not detected in any cat. Kinetic ELISA results were significantly higher for infected cats, than for uninfected cats. Cats infected with different Helicobacter spp. showed similar distribution of OD/min values. There were no effects of age or clinical signs on the results of kinetic ELISA. No correlation between colonization density and seroconversion was observed. There were statistically significant, but weak correlations between the degree of seroconversion and the degree of inflammation, and the number of lymphoid follicles. Infected cats had more severe inflammation in the pylorus and fundus than uninfected cats. Infected sick cats had a higher degree of pyloric, but not fundic inflammation, than healthy infected cats and uninfected sick cats. The results indicate that naturally acquired infection with gastric Helicobacter spp. is associated with seroconversion (IgG) in cats. The similar ELISA values in cats infected with a variety of Helicobacter spp. suggests substantial antigenic homology between different Helicobacter spp. The higher degree of inflammation in infected than uninfected cats, supports a role for Helicobacter as a cause of gastritis in cats.

Antral nodularity identifies children infected with Helicobacter pylori with higher grades of gastric inflammation

Background: The endoscopic pattern of antral nodularity is a peculiar finding in children with Helicobacter pylori infection. The aim of this study was to determine whether this finding is related to more severe gastritis. Methods: One hundred seventy-four consecutive children (median age 8.7 years) referred for gastroscopy were studied. Biopsy specimens from the antrum and body of the stomach were taken to assess H pylori status, gastritis score, and lymphoid follicles. Clinical diagnosis, major symptoms and endoscopic findings were recorded. Results: Eighty-four (48%) children (median age 10.5 years) had evidence of H pylori infection. The endoscopic pattern of antral nodularity was found only in children infected with H pylori (34/84, 40.5% vs. 0/90, 0%, p < 0.0001% 100% specificity, 40.5% sensitivity). Among all children infected with H pylori, the gastritis score was higher (p < 0.0001) in those with antral nodularity (n = 34) than in those without (n = 50). Completely normal gastric mucosal histology was never found in children infected with H pylori with antral nodularity. The presence and number of lymphoid follicles was strongly related to the finding of antral nodularity (p < 0.01). Conclusions: The endoscopic pattern of antral nodularity identifies children with H pylori infection, severe gastritis, and increased lymphoid follicles. (Gastrointest Endosc 2001;53:60-4.)

Histopathological and immunohistological analyses in IgA deficient lymphoplasia (aly/aly) mouse.

The aly/aly mouse has a severe immunodeficiency, because it lacks peripheral lymph nodes as well as IgA and IgG immunoglobulin synthesis. In the present study, we performed histopathological and immunohistological examinations to clarify histological disorders of various immune organs in these mice. Carbon CH40 injections into the apex of the tongue confirmed the absence of submandibular lymph nodes in aly/aly mice. The thymus had a poorly constructed cortex and medulla, and the number of lymphoid follicles was clearly decreased in the spleen. No IgG- or IgA- producing cells were found in any immune organs, including the mucosal immune sites, though several IgM -producing cells were identified. Other characteristic findings included perivascular lymphocytes accumulation in the salivary glands, lungs, liver and pancreas, which caused tissues damage. These results demonstrated that the various lymphoid tissues disorders and organ-specific lymphocyte infiltration cause immuno-deficiency in the aly/aly mouse.

Helicobacter felis infection in dogs: effect on gastric structure and function.

The relationship of Helicobacter felis, an organism that is observed in the stomachs of dogs, to gastric disease in dogs is unclear. The objective of this study was to determine if Helicobacter felis infection alters gastric morphology and gastric secretory function in dogs. Five specific-pathogen-free (SPF), Helicobacter-free Beagle dogs were examined before and for 26 weeks after inoculation with H. felis (ATCC 49179). Three SPF uninfected dogs served as controls. All five dogs became colonized by H. felis as determined by urease activity, histopathology, polymerase chain reaction, and transmission electron microscopic examination of serial gastric biopsies. The degree of colonization ranged from < 1 organism/400 x field to > 10 organisms/400 x field. The fundus, body, and cardia were most heavily colonized. Evaluation of gastric biopsies showed mild gastric inflammation and lymphoid follicles in both infected and uninfected dogs. There was no correlation between the number of organisms observed and the degree of gastric inflammation or number of lymphoid follicles. The gastric secretory axis, assessed by fasting and meal-stimulated plasma gastrin, mucosal gastrin and somatostatin immunoreactivity, fasting gastric pH, and pentagastrin-stimulated gastric acid secretion, was similar in both infected and uninfected dogs. Fasting gastric pH was not a reliable indicator of gastric secretory function. These findings suggest that H. felis may not be a gastric pathogen in dogs. However, the density of colonization and limited duration of infection should be considered when interpreting these findings.

Development of immune complex trapping: experimental study of lymphoid follicles and germinal centers newly induced by exogenous stimulants in mouse popliteal lymph nodes.

The development of immune complex trapping in newly-induced lymphoid follicles of draining popliteal lymph nodes was investigated in young adult mice, which had been given bilateral injection of hemocyanin (KLH) or phytohemagglutinin (PHA), each absorbed onto alumina. HRP-anti-HRP immune complex was injected into the footpad 1 day before sacrifice. Using three series of semi-serial cryostat sections prepared from each popliteal node, the number of lymphoid follicles in each node was counted, and follicular localization of the in vivo injected and in vitro applied immune complexes in each follicle was determined. By day 5, a large germinal center had developed within each preexisting follicle. A large number of 'new' secondary follicles, each containing a small PNA-positive germinal center, appeared outside pre-existing follicles, from day 5 through day 11 in KLH-treated nodes, and from day 7 through day 14 in PHA-treated nodes. Shortly after their appearance, new secondary follicles showed no in vitro or in vivo trapping, but subsequently, many of the new follicles began to display in vitro trapping, at first weakly but later intensely. Occurrence of in vivo trapping in new follicles took some time and was first recognized when new follicles showed intense in vitro trapping. At day 21 or 25, many of the new follicles showed both in vitro and in vivo trapping. It was concluded that in lymph nodes treated with a stimulant, secondary follicles containing germinal centers can be formed de novo in the extrafollicular zone where the follicular trapping microenvironment is absent, but subsequently the microenvironment capable of trapping immune complexes develops at the site of formation of new follicles.

Splenic “Regeneration” after Partial Splenectomy for Gaucher Disease: Histological Features

ABSTRACT: Partial splenectomy for Gaucher disease is often followed by reenlargement of the splenic remnant. It remains unclear if this process is due to tissue regeneration or to continued deposition of glucocerebroside in the reticuloendothelial system or both. We compared the splenic architecture before and after reenlargement in three cases of failed repeated partial splenectomy after two, six and five years. Using the number of lymphoid follicles per hundred low power fields (LF/LPF) as an arbitrary index, we found that prior to the first operation 18, 20 and 27 lymphoid follicles were present per one hundred low power fields, while at the second operation, the corresponding rates were 11, 15 and 17; in control spleens, an average of 712.5 lymphoid follicles were present in one hundred low power fields. The difference in the LF/LPF ratio before and after reenlargement, led us to speculate that splenic re-enlargement in Gaucher disease is mainly the result of the continued deposition of the glucocerebroside in the reticuloendothelial system of the splenic remnant, though some degree of true regeneration as well cannot be completely ruled out. These findings are compared with animal studies and results for partial splenectomy on humans, performed for trauma. Further studies in patients with Gaucher disease are warranted to better define the underlying mechanism of splenic reenlargement.

Splenic adherent cells, stimulated in vitro, induce the reactive formation of lymphoid follicles and germinal centres in draining lymph nodes after subcutaneous transfusion into syngeneic mice.

The reactive formation of lymphoid follicles and germinal centres in lymph nodes, induced by subcutaneous transfer of in vitro activated splenic adherent cells into syngeneic mice, were studied. Adherent cells were obtained by incubating spleen cell suspensions for 24 h and activated by incubating for 1 h in the medium containing keyhole limpet haemocyanin (KLH) absorbed onto alumina. Some of the treated adherent cells were irradiated with 10 Gy x-rays, while others were either not stimulated or were stimulated with alumina-KLH but killed by repeated freezing and thawing. Examination of adherent cell smears immunostained with antibodies against, F4/80, Mac-1, Mac-2 and NLDC-145 indicated that many adherent cells displayed macrophage markers but few displayed the interdigitating cell marker. Animals transfused with KLH-treated adherent cells with or without irradiation showed a marked increase in the number of lymphoid follicles and germinal centres in draining lymph nodes, whereas those transfused with adherent cells which had not been KLH-treated or which had been killed after KLH treatment displayed no significant change in the number of follicles. These results were interpreted as indicating that following transfusion, antigen-activated adherent macrophages migrated into the draining lymph nodes and induced the reactive formation of lymphoid follicles and germinal centres outside preexisting follicles.

Postnatal development of lymphoid follicles in rat Peyer's patches, with special reference to increased follicle number.

The postnatal development of Peyer's patches was investigated using routine histological and immunohistochemical techniques, focusing especially on the formation and increase in number of lymphoid follicles. In addition, we studied the influence on the development of lymphoid follicles in Peyer's patches of a sublethal dose of whole-body X-irradiation at an earlier postnatal age. At 1 day after birth, surface-IgM (sIgM)-bearing cells (B lymphocytes) were scattered throughout the Peyer's patch. At Day 3, sIgM-bearing cells had accumulated to form primary follicles in association with domed elevations. OX2-positive reticular cells (FDC) were detected in the centers of primary follicles at Day 5. The first appearance of germinal centers within lymphoid follicles was noted at 18 days, and at 21 days almost every follicle contained a germinal center. At Day 5, each Peyer's patch contained 6-8 lymphoid follicles, with the lymphoid follicles subsequently increasing in size and number. The mean number of follicles per Peyer's patch became 11.1, the adult level, at 21 days, and remained at this level for the next 15 weeks, even though respective follicles continued to enlarge during the observation period. Three-week-old rats received 400 rad whole-body X-irradiation. At 3 and 7 days after treatment, lymphocytes were largely depleted from Peyer's patches, leaving behind the structural framework of the lymphoid follicles, interfollicular zones and domes. Stromal cells in the follicle remnants retained a positive reaction to OX2.(ABSTRACT TRUNCATED AT 250 WORDS)