The design of a core-shell metal-organic framework comprising a porous bio-MOF-11/14 mixed core and a less porous bio-MOF-14 shell is reported. The growth of the MOF shell was directly observed and supported by SEM and PXRD. The resulting core-shell material exhibits 30% higher CO2 uptake than bio-MOF-14 and low N2 uptake in comparison to the core. When the core-shell architecture is destroyed by fracturing the crystallites via grinding, the amount of N2 adsorbed doubles but the CO2 adsorption capacity remains the same. Finally, the more water stable bio-MOF-14 shell serves to prevent degradation of the water-sensitive core in aqueous environments, as evidenced by SEM and PXRD.

An isoreticular series of cobalt-adeninate bio-MOFs (bio-MOFs-11-14) is reported. The pores of bio-MOFs-11-14 are decorated with acetate, propionate, butyrate, and valerate, respectively. The nitrogen (N 2 ) and carbon dioxide (CO 2 ) adsorption properties of these materials are studied and compared. The isosteric heats of adsorption for CO 2 are calculated, and the CO 2 : N 2 selectivities for each material are determined. As the lengths of the aliphatic chains decorating the pores in bio-MOFs-11-14 increase, the BET surface areas decrease from 1148 m 2 g À1 to 17 m 2 g À1 while the CO 2 : N 2 selectivities predicted from ideal adsorbed solution theory at 1 bar and 273 K for a 10 : 90 CO 2 : N 2 mixture range from 73 : 1

OBJECTIVE Chlamydia trachomatis Infections are a significant cause of reproductive tract pathology. Protective and pathologic immune mediators must be differentiated in order to design a safe and effective vaccine. METHODS Wild-type mice and mice deficient in IL-22 and IL-23 were infected intravaginally with Chlamydia muridarum and their course of infection and oviduct pathology were compared. Local genital tract and draining lymph node immune responses were also examined in IL-23 deficient mice. RESULTS IL-22 and IL-23 deficient mice exhibited normal susceptibility to infection and oviduct pathology. IL-23 was required for development of a Chlamydia-specific Th17 response in the lymph nodes and for production of IL-22 and IL-17 in the genital tract. However, influx of Th1 and innate immune cells was not compromised in the absence of IL-23. CONCLUSIONS IL-22 and IL-23 play either redundant or minimal roles in the pathogenesis of Chlamydia infection in the mouse model. Induction of Th17-associated cytokines by a Chlamydia vaccine should be avoided since these responses are not central to resolution of infection and have pathologic potential.

e Rhesus macaques were studied to directly address the potential for plasmid-deficient Chlamydia trachomatis to serve as a live attenuated vaccine in the genital tract. Five repeated cervical inoculations of rhesus macaques with wild-type serovar D strain D/UW-3/Cx or a plasmid-deficient derivative of this strain, CTD153, resulted in infections with similar kinetics and induced comparable levels of protective immunity. After all animals received five challenges with D/UW-3/Cx, levels of inflammation observed grossly and histologically were similar between the groups. Animals in both groups developed evidence of oviduct dilatation; however, reduced oviduct dilatation was observed for "controllers," i.e., animals without detectable chlamydial DNA in the fimbriae at weeks 5 and 12. Grouping animals into "ascenders" and "controllers" revealed that elevated early T cell responses were associated with protection, whereas higher antibody responses were associated with ascension. Protected animals shared common major histocompatibility complex (MHC) alleles. Overall, genetic differences of individual animals, rather than the presence or absence of the chlamydial plasmid in the primary infecting strain, appeared to play a role in determining the outcome of infection. Infections with the obligate intracellular bacterium Chlamydia trachomatis are a major public health concern. In developing nations, repeated conjunctival infections with serovars A to C cause trachoma, the leading cause of preventable blindness worldwide (1). Genitourinary infections with serovars D to K and L1 to L3 are the most prevalent sexually transmitted bacterial infections in the world. An effective vaccine is not available, and increased screening and treatment have been associated with a rise in the incidence of chlamydial genital tract infection (2). Although antibiotic therapy effectively eliminates infection, it does not reverse established pathology. Serious sequelae resulting from genital tract infection with Chlamydia include pelvic inflammatory disease (PID), ectopic pregnancy, chronic pelvic pain, and infertility in women (reviewed in reference 3). Since the majority of infected women are asymptomatic and do not seek treatment, the consequences of infection often do not become apparent until years after infection, when affected women are unable to conceive.An effective immune response is required for resolution of infection, but overly robust immune activation is responsible for Chlamydia-induced pathology. Studies of mice and guinea pigs have clearly demonstrated that innate immune responses cause tissue damage, while CD4 ϩ T cells and antibody provide protection against challenge infection (reviewed in reference 4). Although specific mediators of protection have been more difficult to delineate for women, correlations between increased CD4 ϩ T cell gamma interferon (IFN-␥) responses and reduced antichlamydial antibody levels have been associated with disease control (reviewed in reference 4). The outcome of a chlamydial infection results...

CD4 T cells and antibody are required for optimal acquired immunity to genital tract infection, and T cell-mediated gamma interferon (IFN-γ) production is necessary to clear infection in the absence of humoral immunity. However, the role of T cell-independent immune responses during primary infection remains unclear. We investigated this question by inoculating wild-type and immune-deficient mice with CM001, a clonal isolate capable of enhanced extragenital replication. Genital inoculation of wild-type mice resulted in transient dissemination to the lungs and spleen that then was rapidly cleared from these organs. However, CM001 genital infection proved lethal for and mice, in which IFN-γ signaling was absent, and for mice, which lacked T and B cells and in which innate IFN-γ signaling was retained. In contrast, B cell-deficient muMT mice, which can generate a Th1 response, and T cell-deficient mice with intact B cell and innate IFN-γ signaling survived. These data collectively indicate that IFN-γ prevents lethal CM001 dissemination in the absence of T cells and suggests a B cell corequirement. Adoptive transfer of convalescent-phase immune serum but not naive IgM to mice infected with CM001 significantly increased the survival time, while transfer of naive B cells completely rescued mice from CM001 lethality. Protection was associated with a significant reduction in the lung chlamydial burden of genitally infected mice. These data reveal an important cooperation between T cell-independent B cell responses and innate IFN-γ in chlamydial host defense and suggest that interactions between T cell-independent antibody and IFN-γ are essential for limiting extragenital dissemination.