To determine whether luteinizing hormone receptors (LHRs) are expressed in canine femoral head subchondral bone (FHSB), hip joint round ligament (RL), cranial cruciate ligament (CCL), and femorotibial joint synovium (FJS) specimens.
1 specimen each of the FHSB, RL, CCL, and FJS obtained from the left hind limbs of 19 fresh canine cadavers.
1 section of each FHSB, RL, CCL, and FJS specimen was processed with rabbit polyclonal IgG anti-human LHR antibody, and 1 section was treated with negative control reagents. Percentage immunoexpression of LHRs in FHSB and FJS sections was analyzed by assessment of 100 bone marrow cells or synoviocytes in 3 adjacent hpf (400×). In each RL and CCL section, immunoexpression of LHRs in fibrocytes was semiquantitatively analyzed on the basis of the mean of the product of percentage staining score (from 0 [no staining] to 3 [> 50% of cells stained]) and staining intensity score (from 0 [no staining] to 2 [moderate to strong staining]) for 3 adjacent hpf.
All tissues examined had variable LHR expression. Expression of LHRs in FHSB, CCL, or FJS specimens did not differ between sexes or between sexually intact and gonadectomized dogs. However, RL specimens from female dogs had significantly greater LHR expression scores, compared with findings for male dogs.
CONCLUSIONS AND CLINICAL RELEVANCE
Results indicated that LHRs are expressed in structural support tissues of canine hip and femorotibial joints. Further research is required to determine the LHRs' function, mechanism of action, and potential contribution to the pathogenesis of hip dysplasia or CCL rupture in dogs.
To determine luteinizing hormone receptor (LHR) expression and response to LHR activation in isolated canine splenic hemangiosarcoma cell lines in vitro.
In vitro cultures of commercially available canine splenic hemangiosarcoma cell lines (EFS, GRACE-HSA, and DAL-4).
The percentage of each cell line expressing LHR was determined by immunocytochemistry. Cells were then treated with increasing doses (7.5 ng/mL, 75 ng/mL) of recombinant canine luteinizing hormone (cLH) for 48 hours and evaluated using a cell proliferation assay.
The percentage of cells expressing LHR was 17.2 ± 4.5%, 11.8 ± 3.1%, and 6.9 ± 2.5% in EFS, GRACE-HSA, and DAL-4, respectively. There was significant increase in cell count in the DAL-4 and EFS cell lines following a 48-hour incubation at the highest cLH concentration (P = .028 and P = .019, respectively). There was not a significant increase in cell count in the GRACE-HSA cell line at either cLH concentration.
Activation of LHR results in cell proliferation in some canine splenic hemangiosarcoma cell lines. These results may explain why spayed and castrated dogs with high circulating LH concentrations may develop hemangiosarcoma more frequently than intact dogs.
To investigate luteinizing hormone (LH) receptor expression in canine nonneoplastic and neoplastic lymph nodes, circulating nonneoplastic lymphocytes, and T-cell lymphoma (TCL) cell lines.
Formalin-fixed, paraffin-embedded lymph nodes (5 neoplastic and 3 nonneoplastic) from 6 dogs, circulating lymphocytes from venous blood specimens obtained from 12 healthy dogs, and 3 TCL cell lines derived from 3 dogs with primary lymphoma.
Lymph node specimens were immunohistochemically stained for determination of LH receptor expression. Circulating nonneoplastic lymphocytes and TCL cell lines were evaluated for LH receptor expression by use of flow cytometry; circulating lymphocytes were also immunophenotyped. The mean percentage of cells positive for LH receptors was determined for each type of specimen. For the healthy dogs, percentages of circulating B and T lymphocytes that expressed LH receptors were assessed on the basis of sex and reproductive status.
The mean percentage of LH receptor-positive cells in canine neoplastic and nonneoplastic lymph nodes was 12.4% and 4.1%, respectively. For the healthy dogs, the mean percentage of circulating LH receptor-positive T lymphocytes was significantly higher in gonadectomized dogs (16.6%) than in sexually intact dogs (10.5%); the percentages of circulating LH receptor-positive B lymphocytes did not significantly differ by reproductive status. Among the 3 canine TCL cell lines, LH receptor expression ranged from 10% to 45%.
CONCLUSIONS AND CLINICAL RELEVANCE
In this study, LH receptor expression by canine neoplastic and nonneoplastic lymphocytes was detected. Research into the effects of downregulation of LH receptor activation in dogs with lymphoma is warranted.
Objective—To determine whether results of cytologic evaluation of preputial epithelial cells correspond to results of a serum endocrine hormone assay and clinical signs associated with adrenocortical disease in castrated ferrets.
Animals—13 clinically normal ferrets and 8 ferrets with signs of adrenocortical disease.
Procedures—Blood and preputial lavage samples were collected from each ferret. Serum samples were submitted to the University of Tennessee Veterinary Diagnostic Laboratory for performance of an endocrine hormone assay. Differential epithelial cell counts were performed on preputial lavage samples to determine the percentage of cornified cells. Results of cytologic evaluation were compared with results of the endocrine hormone assay and clinical status of ferrets.
Results—The percentage of cornified preputial epithelial cells was not significantly correlated with serum 17B-estradiol or androstenedione concentration but was significantly correlated with serum 17-hydroxyprogesterone concentration (r = 0.60). The percentage of cornified preputial epithelial cells was higher in ferrets with clinical signs of adrenocortical disease (mean ± SD, 71.3 ± 16.9%) than in clinically normal ferrets (55.5 ± 19.0%).
Conclusions and Clinical Relevance—Cornification of preputial epithelial cells was correlated with an increase in serum 17-hydroxyprogesterone concentration as well as clinical signs of adrenocortical disease in castrated ferrets. Additional investigation is needed to elucidate the mechanism of preputial epithelial cell cornification in castrated ferrets.
Objective—To determine humoral responses to an
equine West Nile virus (WNV) vaccine in healthy
alpacas and llamas and compare responses in alpacas
and llamas with responses in horses.
Animals—28 alpacas, 56 llamas, and 16 horses.
Procedure—Horses received 2 vaccinations at 4-
week intervals, and alpacas and llamas received 3
vaccinations at 3-week intervals. Fifty-five llamas
received a fourth vaccination 3 weeks after the third.
Blood samples were collected immediately prior to
each vaccination, 3 weeks after the last vaccination
for alpacas and llamas, and 4 weeks after the last vaccination
for horses and tested for virus-neutralizing
antibodies. Samples from 29 randomly selected vaccinated
llamas were used.
Results—None of the animals developed any local or
systemic adverse reactions. Four of 28 (14%) alpacas,
4 of 29 (14%) llamas, and 7 of 16 (44%) horses were
seropositive 3 (llamas and alpacas) or 4 (horses)
weeks after administration of the first vaccination; 27
of 28 (96%) alpacas, 26 of 29 (90%) llamas, and 15 of
16 (94%) horses were seropositive after administration
of the second vaccination; and all 28 alpacas and
28 of 29 (97%) llamas were seropositive 3 weeks
after administration of the third vaccination.
Conclusions and Clinical Relevance—Results suggest
that vaccination with the equine WNV vaccine is
safe in alpacas and llamas. Administration of 3 vaccinations
generally resulted in virus-neutralizing antibody
titers similar to those observed following 2 vaccinations
in horses; however, because it is not known
what antibody titer would be protective against clinical
WNV disease in alpacas or llamas, we cannot conclude
that the vaccine was efficacious. ( J Am Vet Med